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Erschienen in: Inflammation 5/2022

07.04.2022 | Review

Role of High Mobility Group Box 1 in Cardiovascular Diseases

verfasst von: Souad Belmadani, Khalid Matrougui

Erschienen in: Inflammation | Ausgabe 5/2022

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Abstract

High Mobility Group Box 1 (HMGB1) is a ubiquitous, highly conserved nuclear and cytosolic protein that has diverse biological roles depending on its cellular location and posttranslational modifications. The HMGB1 is localized in the nucleus but can be translocated to the cytoplasm to modulate the intracellular signaling and eventually secreted outside the cells. It is widely established that HMGB1 plays a key role in inflammation; however, the role of HMGB1 in the cardiovascular diseases is not well understood. In this review, we will discuss the latest reports on the pathophysiological link between HMGB1 and cardiovascular complications, with special emphasis on the inflammation. Thus, the understanding of the role of HMGB1 may provide new insights into developing new HMGB1-based therapies.
Literatur
1.
Zurück zum Zitat Goodwin, G.H., C. Sanders, and E.W. Johns. 1973. A new group of chromatin-associated proteins with a high content of acidic and basic amino acids. European Journal of Biochemistry 38: 14–19.PubMedCrossRef Goodwin, G.H., C. Sanders, and E.W. Johns. 1973. A new group of chromatin-associated proteins with a high content of acidic and basic amino acids. European Journal of Biochemistry 38: 14–19.PubMedCrossRef
2.
Zurück zum Zitat Calogero, S., F. Grassi, A. Aguzzi, T. Voigtländer, P. Ferrier, S. Ferrari, et al. 1999. The lack of chromosomal protein Hmg1 does not disrupt cell growth but causes lethal hypoglycaemia in newborn mice. Nature Genetics 22: 276–280.PubMedCrossRef Calogero, S., F. Grassi, A. Aguzzi, T. Voigtländer, P. Ferrier, S. Ferrari, et al. 1999. The lack of chromosomal protein Hmg1 does not disrupt cell growth but causes lethal hypoglycaemia in newborn mice. Nature Genetics 22: 276–280.PubMedCrossRef
3.
Zurück zum Zitat Tang, D., R. Kang, W. Xiao, H. Wang, S.K. Calderwood, and X. Xiao. 2007. The anti-inflammatory effects of heat shock protein 72 involve inhibition of high-mobility-group box 1 release and proinflammatory function in macrophages. The Journal of Immunology 179: 1236–1244.PubMedCrossRef Tang, D., R. Kang, W. Xiao, H. Wang, S.K. Calderwood, and X. Xiao. 2007. The anti-inflammatory effects of heat shock protein 72 involve inhibition of high-mobility-group box 1 release and proinflammatory function in macrophages. The Journal of Immunology 179: 1236–1244.PubMedCrossRef
4.
Zurück zum Zitat Scaffidi, P., T. Misteli, and M.E. Bianchi. 2002. Release of chromatin protein HMGB1 by necrotic cells triggers inflammation. Nature 418: 191–195.PubMedCrossRef Scaffidi, P., T. Misteli, and M.E. Bianchi. 2002. Release of chromatin protein HMGB1 by necrotic cells triggers inflammation. Nature 418: 191–195.PubMedCrossRef
5.
Zurück zum Zitat Wakabayashi, A., M. Shimizu, E. Shinya, and H. Takahashi. 2018. HMGB1 released from intestinal epithelia damaged by cholera toxin adjuvant contributes to activation of mucosal dendritic cells and induction of intestinal cytotoxic T lymphocytes and IgA. Cell Death & Disease 9: 631.CrossRef Wakabayashi, A., M. Shimizu, E. Shinya, and H. Takahashi. 2018. HMGB1 released from intestinal epithelia damaged by cholera toxin adjuvant contributes to activation of mucosal dendritic cells and induction of intestinal cytotoxic T lymphocytes and IgA. Cell Death & Disease 9: 631.CrossRef
6.
Zurück zum Zitat Yang, H., D.J. Antoine, U. Andersson, and K.J. Tracey. 2013. The many faces of HMGB1: Molecular structure-functional activity in inflammation, apoptosis, and chemotaxis. Journal of Leukocyte Biology 93: 865–873.PubMedPubMedCentralCrossRef Yang, H., D.J. Antoine, U. Andersson, and K.J. Tracey. 2013. The many faces of HMGB1: Molecular structure-functional activity in inflammation, apoptosis, and chemotaxis. Journal of Leukocyte Biology 93: 865–873.PubMedPubMedCentralCrossRef
7.
Zurück zum Zitat Yang, H., H. Wang, S.S. Chavan, and U. Andersson. 2015. High Mobility Group Box Protein 1 (HMGB1): The prototypical endogenous danger molecule. Molecular Medicine 21 (Suppl 1): S6-s12.PubMedPubMedCentralCrossRef Yang, H., H. Wang, S.S. Chavan, and U. Andersson. 2015. High Mobility Group Box Protein 1 (HMGB1): The prototypical endogenous danger molecule. Molecular Medicine 21 (Suppl 1): S6-s12.PubMedPubMedCentralCrossRef
8.
Zurück zum Zitat Stumbo, A.C., E. Cortez, C.A. Rodrigues, M. Henriques, L.C. Porto, H.S. Barbosa, et al. 2008. Mitochondrial localization of non-histone protein HMGB1 during human endothelial cell-Toxoplasma gondii infection. Cell Biology International 32: 235–238.PubMedCrossRef Stumbo, A.C., E. Cortez, C.A. Rodrigues, M. Henriques, L.C. Porto, H.S. Barbosa, et al. 2008. Mitochondrial localization of non-histone protein HMGB1 during human endothelial cell-Toxoplasma gondii infection. Cell Biology International 32: 235–238.PubMedCrossRef
9.
Zurück zum Zitat Malarkey, C.S., and M.E. Churchill. 2012. The high mobility group box: The ultimate utility player of a cell. Trends in Biochemical Sciences 37: 553–562.PubMedPubMedCentralCrossRef Malarkey, C.S., and M.E. Churchill. 2012. The high mobility group box: The ultimate utility player of a cell. Trends in Biochemical Sciences 37: 553–562.PubMedPubMedCentralCrossRef
10.
Zurück zum Zitat Wahid, A., W. Chen, X. Wang, and X. Tang. 2021. High-mobility group box 1 serves as an inflammation driver of cardiovascular disease. Biomedicine and Pharmacotheraphy 139:111555. Wahid, A., W. Chen, X. Wang, and X. Tang. 2021. High-mobility group box 1 serves as an inflammation driver of cardiovascular disease. Biomedicine and Pharmacotheraphy 139:111555.
11.
Zurück zum Zitat Magna, M., and D.S. Pisetsky. 2014. The role of HMGB1 in the pathogenesis of inflammatory and autoimmune diseases. Molecular Medicine 20: 138–146.PubMedPubMedCentralCrossRef Magna, M., and D.S. Pisetsky. 2014. The role of HMGB1 in the pathogenesis of inflammatory and autoimmune diseases. Molecular Medicine 20: 138–146.PubMedPubMedCentralCrossRef
12.
Zurück zum Zitat Lu, B., D.J. Antoine, K. Kwan, P. Lundbäck, H. Wähämaa, H. Schierbeck, et al. 2014. JAK/STAT1 signaling promotes HMGB1 hyperacetylation and nuclear translocation. Proceedings of the National Academy of Sciences of the United States of America 111: 3068–3073.PubMedPubMedCentralCrossRef Lu, B., D.J. Antoine, K. Kwan, P. Lundbäck, H. Wähämaa, H. Schierbeck, et al. 2014. JAK/STAT1 signaling promotes HMGB1 hyperacetylation and nuclear translocation. Proceedings of the National Academy of Sciences of the United States of America 111: 3068–3073.PubMedPubMedCentralCrossRef
13.
Zurück zum Zitat Andersson, U., H. Wang, K. Palmblad, A.C. Aveberger, O. Bloom, H. Erlandsson-Harris, et al. 2000. High mobility group 1 protein (HMG-1) stimulates proinflammatory cytokine synthesis in human monocytes. Journal of Experimental Medicine 192: 565–570.PubMedPubMedCentralCrossRef Andersson, U., H. Wang, K. Palmblad, A.C. Aveberger, O. Bloom, H. Erlandsson-Harris, et al. 2000. High mobility group 1 protein (HMG-1) stimulates proinflammatory cytokine synthesis in human monocytes. Journal of Experimental Medicine 192: 565–570.PubMedPubMedCentralCrossRef
14.
Zurück zum Zitat Kim, J.B., J. Sig Choi, Y.M. Yu, K. Nam, C.S. Piao, S.W. Kim, et al. 2006. HMGB1, a novel cytokine-like mediator linking acute neuronal death and delayed neuroinflammation in the postischemic brain. Journal of Neuroscience 26: 6413–6421.PubMedCrossRef Kim, J.B., J. Sig Choi, Y.M. Yu, K. Nam, C.S. Piao, S.W. Kim, et al. 2006. HMGB1, a novel cytokine-like mediator linking acute neuronal death and delayed neuroinflammation in the postischemic brain. Journal of Neuroscience 26: 6413–6421.PubMedCrossRef
15.
Zurück zum Zitat Wang, C., J. Jiang, X. Zhang, L. Song, K. Sun, and R. Xu. 2016. Inhibiting HMGB1 reduces cerebral ischemia reperfusion injury in diabetic mice. Inflammation 39: 1862–1870.PubMedCrossRef Wang, C., J. Jiang, X. Zhang, L. Song, K. Sun, and R. Xu. 2016. Inhibiting HMGB1 reduces cerebral ischemia reperfusion injury in diabetic mice. Inflammation 39: 1862–1870.PubMedCrossRef
16.
Zurück zum Zitat Andersson, U., H. Yang, and H. Harris. 2018. Extracellular HMGB1 as a therapeutic target in inflammatory diseases. Expert Opinion on Therapeutic Targets 22: 263–277.PubMedCrossRef Andersson, U., H. Yang, and H. Harris. 2018. Extracellular HMGB1 as a therapeutic target in inflammatory diseases. Expert Opinion on Therapeutic Targets 22: 263–277.PubMedCrossRef
17.
Zurück zum Zitat Andersson, U., H. Yang, and H. Harris. 2018. High-mobility group box 1 protein (HMGB1) operates as an alarmin outside as well as inside cells. Seminars in Immunology 38: 40–48.PubMedCrossRef Andersson, U., H. Yang, and H. Harris. 2018. High-mobility group box 1 protein (HMGB1) operates as an alarmin outside as well as inside cells. Seminars in Immunology 38: 40–48.PubMedCrossRef
18.
Zurück zum Zitat Yang, H., H.S. Hreggvidsdottir, K. Palmblad, H. Wang, M. Ochani, J. Li, et al. 2010. A critical cysteine is required for HMGB1 binding to Toll-like receptor 4 and activation of macrophage cytokine release. Proceedings of the National Academy of Sciences of the United States of America 107: 11942–11947.PubMedPubMedCentralCrossRef Yang, H., H.S. Hreggvidsdottir, K. Palmblad, H. Wang, M. Ochani, J. Li, et al. 2010. A critical cysteine is required for HMGB1 binding to Toll-like receptor 4 and activation of macrophage cytokine release. Proceedings of the National Academy of Sciences of the United States of America 107: 11942–11947.PubMedPubMedCentralCrossRef
19.
Zurück zum Zitat Andrassy, M., H.C. Volz, J.C. Igwe, B. Funke, S.N. Eichberger, Z. Kaya, et al. 2008. High-mobility group box-1 in ischemia-reperfusion injury of the heart. Circulation 117: 3216–3226.PubMedCrossRef Andrassy, M., H.C. Volz, J.C. Igwe, B. Funke, S.N. Eichberger, Z. Kaya, et al. 2008. High-mobility group box-1 in ischemia-reperfusion injury of the heart. Circulation 117: 3216–3226.PubMedCrossRef
20.
Zurück zum Zitat Oozawa, S., S. Mori, T. Kanke, H. Takahashi, K. Liu, Y. Tomono, et al. 2008. Effects of HMGB1 on ischemia-reperfusion injury in the rat heart. Circulation Journal 72: 1178–1184.PubMedCrossRef Oozawa, S., S. Mori, T. Kanke, H. Takahashi, K. Liu, Y. Tomono, et al. 2008. Effects of HMGB1 on ischemia-reperfusion injury in the rat heart. Circulation Journal 72: 1178–1184.PubMedCrossRef
21.
Zurück zum Zitat Higashikuni, Y., K. Tanaka, M. Kato, O. Nureki, Y. Hirata, R. Nagai, et al. 2013. Toll-like receptor-2 mediates adaptive cardiac hypertrophy in response to pressure overload through interleukin-1β upregulation via nuclear factor κB activation. Journal of the American Heart Association 2:e000267. Higashikuni, Y., K. Tanaka, M. Kato, O. Nureki, Y. Hirata, R. Nagai, et al. 2013. Toll-like receptor-2 mediates adaptive cardiac hypertrophy in response to pressure overload through interleukin-1β upregulation via nuclear factor κB activation. Journal of the American Heart Association 2:e000267.
22.
Zurück zum Zitat Zhang, L., M. Liu, H. Jiang, Y. Yu, P. Yu, R. Tong, et al. 2016. Extracellular high-mobility group box 1 mediates pressure overload-induced cardiac hypertrophy and heart failure. Journal of Cellular and Molecular Medicine 20: 459–470.PubMedCrossRef Zhang, L., M. Liu, H. Jiang, Y. Yu, P. Yu, R. Tong, et al. 2016. Extracellular high-mobility group box 1 mediates pressure overload-induced cardiac hypertrophy and heart failure. Journal of Cellular and Molecular Medicine 20: 459–470.PubMedCrossRef
23.
Zurück zum Zitat Su, F.F., M.Q. Shi, W.G. Guo, X.T. Liu, H.T. Wang, Z.F. Lu, et al. 2012. High-mobility group box 1 induces calcineurin-mediated cell hypertrophy in neonatal rat ventricular myocytes. Mediators of Inflammation 2012:805149. Su, F.F., M.Q. Shi, W.G. Guo, X.T. Liu, H.T. Wang, Z.F. Lu, et al. 2012. High-mobility group box 1 induces calcineurin-mediated cell hypertrophy in neonatal rat ventricular myocytes. Mediators of Inflammation 2012:805149.
24.
Zurück zum Zitat Funayama, A., T. Shishido, S. Netsu, T. Narumi, S. Kadowaki, H. Takahashi, et al. 2013. Cardiac nuclear high mobility group box 1 prevents the development of cardiac hypertrophy and heart failure. Cardiovascular Research 99: 657–664.PubMedPubMedCentralCrossRef Funayama, A., T. Shishido, S. Netsu, T. Narumi, S. Kadowaki, H. Takahashi, et al. 2013. Cardiac nuclear high mobility group box 1 prevents the development of cardiac hypertrophy and heart failure. Cardiovascular Research 99: 657–664.PubMedPubMedCentralCrossRef
25.
Zurück zum Zitat Limana, F., A. Germani, A. Zacheo, J. Kajstura, A. Di Carlo, G. Borsellino, et al. 2005. Exogenous high-mobility group box 1 protein induces myocardial regeneration after infarction via enhanced cardiac C-kit+ cell proliferation and differentiation. Circulation Research 97: e73-83.PubMedCrossRef Limana, F., A. Germani, A. Zacheo, J. Kajstura, A. Di Carlo, G. Borsellino, et al. 2005. Exogenous high-mobility group box 1 protein induces myocardial regeneration after infarction via enhanced cardiac C-kit+ cell proliferation and differentiation. Circulation Research 97: e73-83.PubMedCrossRef
26.
Zurück zum Zitat Kitahara, T., Y. Takeishi, M. Harada, T. Niizeki, S. Suzuki, T. Sasaki, et al. 2008. High-mobility group box 1 restores cardiac function after myocardial infarction in transgenic mice. Cardiovascular Research 80: 40–46.PubMedCrossRef Kitahara, T., Y. Takeishi, M. Harada, T. Niizeki, S. Suzuki, T. Sasaki, et al. 2008. High-mobility group box 1 restores cardiac function after myocardial infarction in transgenic mice. Cardiovascular Research 80: 40–46.PubMedCrossRef
27.
Zurück zum Zitat Kaya, Z., M. Afanasyeva, Y. Wang, K.M. Dohmen, J. Schlichting, T. Tretter, et al. 2001. Contribution of the innate immune system to autoimmune myocarditis: A role for complement. Nature Immunology 2: 739–745.PubMedCrossRef Kaya, Z., M. Afanasyeva, Y. Wang, K.M. Dohmen, J. Schlichting, T. Tretter, et al. 2001. Contribution of the innate immune system to autoimmune myocarditis: A role for complement. Nature Immunology 2: 739–745.PubMedCrossRef
28.
Zurück zum Zitat Heymans, S. 2006. Inflammation and cardiac remodeling during viral myocarditis. Ernst Schering Research Found Workshop 197–218. Heymans, S. 2006. Inflammation and cardiac remodeling during viral myocarditis. Ernst Schering Research Found Workshop 197–218.
29.
Zurück zum Zitat Eriksson, S., J. Hellman, and K. Pettersson. 2005. Autoantibodies against cardiac troponins. New England Journal of Medicine 352: 98–100.PubMedCrossRef Eriksson, S., J. Hellman, and K. Pettersson. 2005. Autoantibodies against cardiac troponins. New England Journal of Medicine 352: 98–100.PubMedCrossRef
30.
Zurück zum Zitat Göser, S., M. Andrassy, S.J. Buss, F. Leuschner, C.H. Volz, R. Ottl, et al. 2006. Cardiac troponin I but not cardiac troponin T induces severe autoimmune inflammation in the myocardium. Circulation 114: 1693–1702.PubMedCrossRef Göser, S., M. Andrassy, S.J. Buss, F. Leuschner, C.H. Volz, R. Ottl, et al. 2006. Cardiac troponin I but not cardiac troponin T induces severe autoimmune inflammation in the myocardium. Circulation 114: 1693–1702.PubMedCrossRef
31.
Zurück zum Zitat Bangert, A., M. Andrassy, A.M. Müller, M. Bockstahler, A. Fischer, C.H. Volz, et al. 2016. Critical role of RAGE and HMGB1 in inflammatory heart disease. Proceedings of the National Academy of Sciences of the United States of America 113: E155–E164.PubMed Bangert, A., M. Andrassy, A.M. Müller, M. Bockstahler, A. Fischer, C.H. Volz, et al. 2016. Critical role of RAGE and HMGB1 in inflammatory heart disease. Proceedings of the National Academy of Sciences of the United States of America 113: E155–E164.PubMed
32.
Zurück zum Zitat Su, Z., P. Zhang, Y. Yu, H. Lu, Y. Liu, P. Ni, et al. 2016. HMGB1 facilitated macrophage reprogramming towards a proinflammatory M1-like phenotype in experimental autoimmune myocarditis development. Science and Reports 6: 21884.CrossRef Su, Z., P. Zhang, Y. Yu, H. Lu, Y. Liu, P. Ni, et al. 2016. HMGB1 facilitated macrophage reprogramming towards a proinflammatory M1-like phenotype in experimental autoimmune myocarditis development. Science and Reports 6: 21884.CrossRef
33.
Zurück zum Zitat Kohno, T., T. Anzai, K. Naito, T. Miyasho, M. Okamoto, H. Yokota, et al. 2009. Role of high-mobility group box 1 protein in post-infarction healing process and left ventricular remodelling. Cardiovascular Research 81: 565–573.PubMedCrossRef Kohno, T., T. Anzai, K. Naito, T. Miyasho, M. Okamoto, H. Yokota, et al. 2009. Role of high-mobility group box 1 protein in post-infarction healing process and left ventricular remodelling. Cardiovascular Research 81: 565–573.PubMedCrossRef
34.
Zurück zum Zitat Yu, P., M. Liu, B. Zhang, Y. Yu, E. Su, S. Xie, et al. 2020. Cardiomyocyte-restricted high-mobility group box 1 (HMGB1) deletion leads to small heart and glycolipid metabolic disorder through GR/PGC-1α signalling. Cell Death Discov 6: 106.PubMedPubMedCentralCrossRef Yu, P., M. Liu, B. Zhang, Y. Yu, E. Su, S. Xie, et al. 2020. Cardiomyocyte-restricted high-mobility group box 1 (HMGB1) deletion leads to small heart and glycolipid metabolic disorder through GR/PGC-1α signalling. Cell Death Discov 6: 106.PubMedPubMedCentralCrossRef
35.
Zurück zum Zitat Wu, R.N., T.Y. Yu, J.C. Zhou, M. Li, H.K. Gao, C. Zhao, et al. 2018. Targeting HMGB1 ameliorates cardiac fibrosis through restoring TLR2-mediated autophagy suppression in myocardial fibroblasts. International Journal of Cardiology 267: 156–162.PubMedCrossRef Wu, R.N., T.Y. Yu, J.C. Zhou, M. Li, H.K. Gao, C. Zhao, et al. 2018. Targeting HMGB1 ameliorates cardiac fibrosis through restoring TLR2-mediated autophagy suppression in myocardial fibroblasts. International Journal of Cardiology 267: 156–162.PubMedCrossRef
36.
37.
Zurück zum Zitat Hoshina, T., K. Kusuhara, K. Ikeda, Y. Mizuno, M. Saito, and T. Hara. 2008. High mobility group box 1 (HMGB1) and macrophage migration inhibitory factor (MIF) in Kawasaki disease. Scandinavian Journal of Rheumatology 37: 445–449.PubMedCrossRef Hoshina, T., K. Kusuhara, K. Ikeda, Y. Mizuno, M. Saito, and T. Hara. 2008. High mobility group box 1 (HMGB1) and macrophage migration inhibitory factor (MIF) in Kawasaki disease. Scandinavian Journal of Rheumatology 37: 445–449.PubMedCrossRef
38.
Zurück zum Zitat Qian, B., H. Huang, M. Cheng, T. Qin, T. Chen, and J. Zhao. 2020. Mechanism of HMGB1-RAGE in Kawasaki disease with coronary artery injury. European Journal of Medical Research 25: 8.PubMedPubMedCentralCrossRef Qian, B., H. Huang, M. Cheng, T. Qin, T. Chen, and J. Zhao. 2020. Mechanism of HMGB1-RAGE in Kawasaki disease with coronary artery injury. European Journal of Medical Research 25: 8.PubMedPubMedCentralCrossRef
39.
Zurück zum Zitat Jia, C., J. Zhang, H. Chen, Y. Zhuge, H. Chen, F. Qian, et al. 2019. Endothelial cell pyroptosis plays an important role in Kawasaki disease via HMGB1/RAGE/cathespin B signaling pathway and NLRP3 inflammasome activation. Cell Death & Disease 10: 778.CrossRef Jia, C., J. Zhang, H. Chen, Y. Zhuge, H. Chen, F. Qian, et al. 2019. Endothelial cell pyroptosis plays an important role in Kawasaki disease via HMGB1/RAGE/cathespin B signaling pathway and NLRP3 inflammasome activation. Cell Death & Disease 10: 778.CrossRef
40.
Zurück zum Zitat Ueno, K., Y. Nomura, Y. Morita, and Y. Kawano. 2021. Prednisolone suppresses the extracellular release of HMGB-1 and associated inflammatory pathways in Kawasaki disease. Frontiers in Immunology 12:640315. Ueno, K., Y. Nomura, Y. Morita, and Y. Kawano. 2021. Prednisolone suppresses the extracellular release of HMGB-1 and associated inflammatory pathways in Kawasaki disease. Frontiers in Immunology 12:640315.
41.
Zurück zum Zitat Mitola, S., M. Belleri, C. Urbinati, D. Coltrini, B. Sparatore, M. Pedrazzi, et al. 2006. Cutting edge: Extracellular high mobility group box-1 protein is a proangiogenic cytokine. The Journal of Immunology 176: 12–15.PubMedCrossRef Mitola, S., M. Belleri, C. Urbinati, D. Coltrini, B. Sparatore, M. Pedrazzi, et al. 2006. Cutting edge: Extracellular high mobility group box-1 protein is a proangiogenic cytokine. The Journal of Immunology 176: 12–15.PubMedCrossRef
42.
Zurück zum Zitat Frantz, S., K.A. Vincent, O. Feron, and R.A. Kelly. 2005. Innate immunity and angiogenesis. Circulation Research 96: 15–26.PubMedCrossRef Frantz, S., K.A. Vincent, O. Feron, and R.A. Kelly. 2005. Innate immunity and angiogenesis. Circulation Research 96: 15–26.PubMedCrossRef
43.
Zurück zum Zitat Yuan, K., T.M. Hong, J.J. Chen, W.H. Tsai, and M.T. Lin. 2004. Syndecan-1 up-regulated by ephrinB2/EphB4 plays dual roles in inflammatory angiogenesis. Blood 104: 1025–1033.PubMedCrossRef Yuan, K., T.M. Hong, J.J. Chen, W.H. Tsai, and M.T. Lin. 2004. Syndecan-1 up-regulated by ephrinB2/EphB4 plays dual roles in inflammatory angiogenesis. Blood 104: 1025–1033.PubMedCrossRef
44.
Zurück zum Zitat Sachdev, U., X. Cui, G. Hong, S. Namkoong, J.M. Karlsson, C.J. Baty, et al. 2012. High mobility group box 1 promotes endothelial cell angiogenic behavior in vitro and improves muscle perfusion in vivo in response to ischemic injury. Journal of Vascular Surgery 55: 180–191. Sachdev, U., X. Cui, G. Hong, S. Namkoong, J.M. Karlsson, C.J. Baty, et al. 2012. High mobility group box 1 promotes endothelial cell angiogenic behavior in vitro and improves muscle perfusion in vivo in response to ischemic injury. Journal of Vascular Surgery 55: 180–191.
45.
Zurück zum Zitat Sachdev, U., X. Cui, and E. Tzeng. 2013. HMGB1 and TLR4 mediate skeletal muscle recovery in a murine model of hindlimb ischemia. Journal of Vascular Surgery 58: 460–469.PubMedPubMedCentralCrossRef Sachdev, U., X. Cui, and E. Tzeng. 2013. HMGB1 and TLR4 mediate skeletal muscle recovery in a murine model of hindlimb ischemia. Journal of Vascular Surgery 58: 460–469.PubMedPubMedCentralCrossRef
46.
Zurück zum Zitat Lu, B., T. Nakamura, K. Inouye, J. Li, Y. Tang, P. Lundbäck, et al. 2012. Novel role of PKR in inflammasome activation and HMGB1 release. Nature 488: 670–674.PubMedPubMedCentralCrossRef Lu, B., T. Nakamura, K. Inouye, J. Li, Y. Tang, P. Lundbäck, et al. 2012. Novel role of PKR in inflammasome activation and HMGB1 release. Nature 488: 670–674.PubMedPubMedCentralCrossRef
47.
Zurück zum Zitat Xu, J., X. Cui, J. Li, P. Koutakis, I. Pipinos, E. Tzeng, et al. 2018. Chloroquine improves the response to ischemic muscle injury and increases HMGB1 after arterial ligation. Journal of Vascular Surgery 67: 910–921.PubMedCrossRef Xu, J., X. Cui, J. Li, P. Koutakis, I. Pipinos, E. Tzeng, et al. 2018. Chloroquine improves the response to ischemic muscle injury and increases HMGB1 after arterial ligation. Journal of Vascular Surgery 67: 910–921.PubMedCrossRef
48.
Zurück zum Zitat Lan, J., H. Luo, R. Wu, J. Wang, B. Zhou, Y. Zhang, et al. 2020. Internalization of HMGB1 (High Mobility Group Box 1) promotes angiogenesis in endothelial cells. Arteriosclerosis, Thrombosis, and Vascular Biology 40: 2922–2940.PubMedCrossRef Lan, J., H. Luo, R. Wu, J. Wang, B. Zhou, Y. Zhang, et al. 2020. Internalization of HMGB1 (High Mobility Group Box 1) promotes angiogenesis in endothelial cells. Arteriosclerosis, Thrombosis, and Vascular Biology 40: 2922–2940.PubMedCrossRef
49.
Zurück zum Zitat Hansen, L.M., D. Gupta, G. Joseph, D. Weiss, and W.R. Taylor. 2017. The receptor for advanced glycation end products impairs collateral formation in both diabetic and non-diabetic mice. Laboratory Investigation 97: 34–42.PubMedCrossRef Hansen, L.M., D. Gupta, G. Joseph, D. Weiss, and W.R. Taylor. 2017. The receptor for advanced glycation end products impairs collateral formation in both diabetic and non-diabetic mice. Laboratory Investigation 97: 34–42.PubMedCrossRef
50.
Zurück zum Zitat Inoue, K., K. Kawahara, K.K. Biswas, K. Ando, K. Mitsudo, M. Nobuyoshi, et al. 2007. HMGB1 expression by activated vascular smooth muscle cells in advanced human atherosclerosis plaques. Cardiovascular Pathology 16: 136–143.PubMedCrossRef Inoue, K., K. Kawahara, K.K. Biswas, K. Ando, K. Mitsudo, M. Nobuyoshi, et al. 2007. HMGB1 expression by activated vascular smooth muscle cells in advanced human atherosclerosis plaques. Cardiovascular Pathology 16: 136–143.PubMedCrossRef
51.
Zurück zum Zitat Kanellakis, P., A. Agrotis, T.S. Kyaw, C. Koulis, I. Ahrens, S. Mori, et al. 2011. High-mobility group box protein 1 neutralization reduces development of diet-induced atherosclerosis in apolipoprotein e-deficient mice. Arteriosclerosis, Thrombosis, and Vascular Biology 31: 313–319.PubMedCrossRef Kanellakis, P., A. Agrotis, T.S. Kyaw, C. Koulis, I. Ahrens, S. Mori, et al. 2011. High-mobility group box protein 1 neutralization reduces development of diet-induced atherosclerosis in apolipoprotein e-deficient mice. Arteriosclerosis, Thrombosis, and Vascular Biology 31: 313–319.PubMedCrossRef
52.
Zurück zum Zitat Ghaffari, S., E. Jang, F. Naderinabi, R. Sanwal, N. Khosraviani, C. Wang, et al. 2021. Endothelial HMGB1 is a critical regulator of LDL transcytosis via an SREBP2-SR-BI axis. Arteriosclerosis, Thrombosis, and Vascular Biology 41: 200–216.PubMed Ghaffari, S., E. Jang, F. Naderinabi, R. Sanwal, N. Khosraviani, C. Wang, et al. 2021. Endothelial HMGB1 is a critical regulator of LDL transcytosis via an SREBP2-SR-BI axis. Arteriosclerosis, Thrombosis, and Vascular Biology 41: 200–216.PubMed
53.
Zurück zum Zitat Zhao, Y., W. Li, and D. Zhang. Gycyrrhizic acid alleviates atherosclerotic lesions in rats with diabetes mellitus. Molecular Medicine Report 24. Zhao, Y., W. Li, and D. Zhang. Gycyrrhizic acid alleviates atherosclerotic lesions in rats with diabetes mellitus. Molecular Medicine Report 24.
54.
Zurück zum Zitat Li, Y., H. Li, B. Chen, F. Yang, and Z. Hao. 2021. miR-141–5p suppresses vascular smooth muscle cell inflammation, proliferation, and migration via inhibiting the HMGB1/NF-kappaB pathway. Journal of the Biochemical Molecular Toxicology 35:e22828. Li, Y., H. Li, B. Chen, F. Yang, and Z. Hao. 2021. miR-141–5p suppresses vascular smooth muscle cell inflammation, proliferation, and migration via inhibiting the HMGB1/NF-kappaB pathway. Journal of the Biochemical Molecular Toxicology 35:e22828.
55.
Zurück zum Zitat Roshan, M.H., A. Tambo, and N.P. Pace. 2016. The Role of TLR2, TLR4, and TLR9 in the pathogenesis of atherosclerosis. International Journal of the Inflammation 2016: 1532832.CrossRef Roshan, M.H., A. Tambo, and N.P. Pace. 2016. The Role of TLR2, TLR4, and TLR9 in the pathogenesis of atherosclerosis. International Journal of the Inflammation 2016: 1532832.CrossRef
56.
Zurück zum Zitat Pahwa, R., B. Adams-Huet, and I. Jialal. 2017. The effect of increasing body mass index on cardio-metabolic risk and biomarkers of oxidative stress and inflammation in nascent metabolic syndrome. Journal of Diabetes and Its Complications 31: 810–813.PubMedCrossRef Pahwa, R., B. Adams-Huet, and I. Jialal. 2017. The effect of increasing body mass index on cardio-metabolic risk and biomarkers of oxidative stress and inflammation in nascent metabolic syndrome. Journal of Diabetes and Its Complications 31: 810–813.PubMedCrossRef
57.
Zurück zum Zitat Pahwa, R., and I. Jialal. 2016. The role of the high-mobility group box1 protein-Toll like receptor pathway in diabetic vascular disease. Journal of Diabetes and Its Complications 30: 1186–1191.PubMedCrossRef Pahwa, R., and I. Jialal. 2016. The role of the high-mobility group box1 protein-Toll like receptor pathway in diabetic vascular disease. Journal of Diabetes and Its Complications 30: 1186–1191.PubMedCrossRef
58.
Zurück zum Zitat Yan, X.X., L. Lu, W.H. Peng, L.J. Wang, Q. Zhang, R.Y. Zhang, et al. 2009. Increased serum HMGB1 level is associated with coronary artery disease in nondiabetic and type 2 diabetic patients. Atherosclerosis 205: 544–548.PubMedCrossRef Yan, X.X., L. Lu, W.H. Peng, L.J. Wang, Q. Zhang, R.Y. Zhang, et al. 2009. Increased serum HMGB1 level is associated with coronary artery disease in nondiabetic and type 2 diabetic patients. Atherosclerosis 205: 544–548.PubMedCrossRef
59.
Zurück zum Zitat Marjanac, I., R. Lovrić, and J. Barbić. 2019. Serum levels of the high-mobility group box 1 protein (HMGB1) in children with type 1 diabetes mellitus: Case-control study. Central-European Journal of Immunology 44: 33–37.PubMedPubMedCentralCrossRef Marjanac, I., R. Lovrić, and J. Barbić. 2019. Serum levels of the high-mobility group box 1 protein (HMGB1) in children with type 1 diabetes mellitus: Case-control study. Central-European Journal of Immunology 44: 33–37.PubMedPubMedCentralCrossRef
60.
Zurück zum Zitat Giovannini, S., G. Tinelli, F. Biscetti, G. Straface, F. Angelini, D. Pitocco, et al. 2017. Serum high mobility group box-1 and osteoprotegerin levels are associated with peripheral arterial disease and critical limb ischemia in type 2 diabetic subjects. Cardiovascular Diabetology 16: 99.PubMedPubMedCentralCrossRef Giovannini, S., G. Tinelli, F. Biscetti, G. Straface, F. Angelini, D. Pitocco, et al. 2017. Serum high mobility group box-1 and osteoprotegerin levels are associated with peripheral arterial disease and critical limb ischemia in type 2 diabetic subjects. Cardiovascular Diabetology 16: 99.PubMedPubMedCentralCrossRef
61.
Zurück zum Zitat Oozawa, S., S. Sano, and M. Nishibori. 2014. Usefulness of high mobility group box 1 protein as a plasma biomarker in patient with peripheral artery disease. Acta Medica Okayama 68: 157–162.PubMed Oozawa, S., S. Sano, and M. Nishibori. 2014. Usefulness of high mobility group box 1 protein as a plasma biomarker in patient with peripheral artery disease. Acta Medica Okayama 68: 157–162.PubMed
62.
Zurück zum Zitat Biscetti, F., G. Straface, R. De Cristofaro, S. Lancellotti, P. Rizzo, V. Arena, et al. 2010. High-mobility group box-1 protein promotes angiogenesis after peripheral ischemia in diabetic mice through a VEGF-dependent mechanism. Diabetes 59: 1496–1505.PubMedPubMedCentralCrossRef Biscetti, F., G. Straface, R. De Cristofaro, S. Lancellotti, P. Rizzo, V. Arena, et al. 2010. High-mobility group box-1 protein promotes angiogenesis after peripheral ischemia in diabetic mice through a VEGF-dependent mechanism. Diabetes 59: 1496–1505.PubMedPubMedCentralCrossRef
63.
Zurück zum Zitat Volz, H.C., C. Seidel, D. Laohachewin, Z. Kaya, O.J. Müller, S.T. Pleger, et al. 2010. HMGB1: The missing link between diabetes mellitus and heart failure. Basic Research in Cardiology 105: 805–820.PubMedCrossRef Volz, H.C., C. Seidel, D. Laohachewin, Z. Kaya, O.J. Müller, S.T. Pleger, et al. 2010. HMGB1: The missing link between diabetes mellitus and heart failure. Basic Research in Cardiology 105: 805–820.PubMedCrossRef
64.
Zurück zum Zitat Chen, Q., Z.Y. Wang, L.Y. Chen, and H.Y. Hu. 2017. Roles of High Mobility Group Box 1 in cardiovascular calcification. Cellular Physiology and Biochemistry 42: 427–440.PubMedCrossRef Chen, Q., Z.Y. Wang, L.Y. Chen, and H.Y. Hu. 2017. Roles of High Mobility Group Box 1 in cardiovascular calcification. Cellular Physiology and Biochemistry 42: 427–440.PubMedCrossRef
65.
Zurück zum Zitat Wang, B., G. Wei, B. Liu, X. Zhou, H. Xiao, N. Dong, et al. 2016. The role of High Mobility Group Box 1 protein in interleukin-18-induced myofibroblastic transition of valvular interstitial cells. Cardiology 135: 168–178.PubMedCrossRef Wang, B., G. Wei, B. Liu, X. Zhou, H. Xiao, N. Dong, et al. 2016. The role of High Mobility Group Box 1 protein in interleukin-18-induced myofibroblastic transition of valvular interstitial cells. Cardiology 135: 168–178.PubMedCrossRef
66.
Zurück zum Zitat Passmore, M., M. Nataatmadja, Y.L. Fung, B. Pearse, S. Gabriel, P. Tesar, et al. 2015. Osteopontin alters endothelial and valvular interstitial cell behaviour in calcific aortic valve stenosis through HMGB1 regulation. European Journal of Cardio-Thoracic Surgery 48: e20–e29.PubMedCrossRef Passmore, M., M. Nataatmadja, Y.L. Fung, B. Pearse, S. Gabriel, P. Tesar, et al. 2015. Osteopontin alters endothelial and valvular interstitial cell behaviour in calcific aortic valve stenosis through HMGB1 regulation. European Journal of Cardio-Thoracic Surgery 48: e20–e29.PubMedCrossRef
67.
Zurück zum Zitat Wang, Y., J. Shan, W. Yang, H. Zheng, and S. Xue. 2013. High mobility group box 1 (HMGB1) mediates high-glucose-induced calcification in vascular smooth muscle cells of saphenous veins. Inflammation 36: 1592–1604.PubMedCrossRef Wang, Y., J. Shan, W. Yang, H. Zheng, and S. Xue. 2013. High mobility group box 1 (HMGB1) mediates high-glucose-induced calcification in vascular smooth muscle cells of saphenous veins. Inflammation 36: 1592–1604.PubMedCrossRef
68.
Zurück zum Zitat Chen, Z., R. Li, L.G. Pei, Z.H. Wei, J. Xie, H. Wu, et al. 2021. High-mobility group box-1 promotes vascular calcification in diabetic mice via endoplasmic reticulum stress. Journal of Cellular and Molecular Medicine 25: 3724–3734.PubMedPubMedCentralCrossRef Chen, Z., R. Li, L.G. Pei, Z.H. Wei, J. Xie, H. Wu, et al. 2021. High-mobility group box-1 promotes vascular calcification in diabetic mice via endoplasmic reticulum stress. Journal of Cellular and Molecular Medicine 25: 3724–3734.PubMedPubMedCentralCrossRef
69.
Zurück zum Zitat Sun, Y., C.H. Byon, K. Yuan, J. Chen, X. Mao, J.M. Heath, et al. 2012. Smooth muscle cell-specific runx2 deficiency inhibits vascular calcification. Circulation Research 111: 543–552.PubMedPubMedCentralCrossRef Sun, Y., C.H. Byon, K. Yuan, J. Chen, X. Mao, J.M. Heath, et al. 2012. Smooth muscle cell-specific runx2 deficiency inhibits vascular calcification. Circulation Research 111: 543–552.PubMedPubMedCentralCrossRef
70.
Zurück zum Zitat Lin, M.E., T. Chen, E.M. Leaf, M.Y. Speer, and C.M. Giachelli. 2015. Runx2 expression in smooth muscle cells is required for arterial medial calcification in mice. American Journal of Pathology 185: 1958–1969.PubMedPubMedCentralCrossRef Lin, M.E., T. Chen, E.M. Leaf, M.Y. Speer, and C.M. Giachelli. 2015. Runx2 expression in smooth muscle cells is required for arterial medial calcification in mice. American Journal of Pathology 185: 1958–1969.PubMedPubMedCentralCrossRef
71.
Zurück zum Zitat Byon, C.H., A. Javed, Q. Dai, J.C. Kappes, T.L. Clemens, V.M. Darley-Usmar, et al. 2008. Oxidative stress induces vascular calcification through modulation of the osteogenic transcription factor Runx2 by AKT signaling. Journal of Biological Chemistry 283: 15319–15327.PubMedPubMedCentralCrossRef Byon, C.H., A. Javed, Q. Dai, J.C. Kappes, T.L. Clemens, V.M. Darley-Usmar, et al. 2008. Oxidative stress induces vascular calcification through modulation of the osteogenic transcription factor Runx2 by AKT signaling. Journal of Biological Chemistry 283: 15319–15327.PubMedPubMedCentralCrossRef
72.
Zurück zum Zitat Nebbioso, M., A. Lambiase, M. Armentano, G. Tucciarone, V. Bonfiglio, R. Plateroti, et al. 2020. The complex relationship between diabetic retinopathy and High-Mobility Group Box: a review of molecular pathways and therapeutic strategies. Antioxidants (Basel) 9. Nebbioso, M., A. Lambiase, M. Armentano, G. Tucciarone, V. Bonfiglio, R. Plateroti, et al. 2020. The complex relationship between diabetic retinopathy and High-Mobility Group Box: a review of molecular pathways and therapeutic strategies. Antioxidants (Basel) 9.
73.
Zurück zum Zitat Steinle, J.J. 2020. Role of HMGB1 signaling in the inflammatory process in diabetic retinopathy. Cell Signal 73:109687. Steinle, J.J. 2020. Role of HMGB1 signaling in the inflammatory process in diabetic retinopathy. Cell Signal 73:109687.
74.
Zurück zum Zitat El-Asrar, A.M., M.I. Nawaz, D. Kangave, K. Geboes, M.S. Ola, S. Ahmad, et al. 2011. High-mobility group box-1 and biomarkers of inflammation in the vitreous from patients with proliferative diabetic retinopathy. Molecular Vision 17: 1829–1838.PubMedPubMedCentral El-Asrar, A.M., M.I. Nawaz, D. Kangave, K. Geboes, M.S. Ola, S. Ahmad, et al. 2011. High-mobility group box-1 and biomarkers of inflammation in the vitreous from patients with proliferative diabetic retinopathy. Molecular Vision 17: 1829–1838.PubMedPubMedCentral
75.
Zurück zum Zitat Liang, W.J., H.W. Yang, H.N. Liu, W. Qian, and X.L. Chen. 2020. HMGB1 upregulates NF-kB by inhibiting IKB-α and associates with diabetic retinopathy. Life Sciences 241:117146. Liang, W.J., H.W. Yang, H.N. Liu, W. Qian, and X.L. Chen. 2020. HMGB1 upregulates NF-kB by inhibiting IKB-α and associates with diabetic retinopathy. Life Sciences 241:117146.
76.
Zurück zum Zitat Abu El-Asrar, A.M., K. Alam, M. Garcia-Ramirez, A. Ahmad, M.M. Siddiquei, G. Mohammad, et al. 2017. Association of HMGB1 with oxidative stress markers and regulators in PDR. Molecular Vision 23: 853–871.PubMedPubMedCentral Abu El-Asrar, A.M., K. Alam, M. Garcia-Ramirez, A. Ahmad, M.M. Siddiquei, G. Mohammad, et al. 2017. Association of HMGB1 with oxidative stress markers and regulators in PDR. Molecular Vision 23: 853–871.PubMedPubMedCentral
77.
Zurück zum Zitat Jiang, Y., L. Liu, E. Curtiss, and J.J. Steinle. 2017. Epac1 blocks NLRP3 inflammasome to reduce IL-1β in retinal endothelial cells and mouse retinal vasculature. Mediators of Inflammation 2017: 2860956.PubMedPubMedCentral Jiang, Y., L. Liu, E. Curtiss, and J.J. Steinle. 2017. Epac1 blocks NLRP3 inflammasome to reduce IL-1β in retinal endothelial cells and mouse retinal vasculature. Mediators of Inflammation 2017: 2860956.PubMedPubMedCentral
78.
Zurück zum Zitat Jiang, Y., L. Liu, and J.J. Steinle. 2018. Epac1 deacetylates HMGB1 through increased IGFBP-3 and SIRT1 levels in the retinal vasculature. Molecular Vision 24: 727–732.PubMedPubMedCentral Jiang, Y., L. Liu, and J.J. Steinle. 2018. Epac1 deacetylates HMGB1 through increased IGFBP-3 and SIRT1 levels in the retinal vasculature. Molecular Vision 24: 727–732.PubMedPubMedCentral
79.
Zurück zum Zitat Jiang, Y., and J.J. Steinle. 2020. Epac1 requires AMPK phosphorylation to regulate HMGB1 in the retinal vasculature. Investigative Ophthalmology & Visual Science 61: 33.CrossRef Jiang, Y., and J.J. Steinle. 2020. Epac1 requires AMPK phosphorylation to regulate HMGB1 in the retinal vasculature. Investigative Ophthalmology & Visual Science 61: 33.CrossRef
80.
Zurück zum Zitat Liu, L., Y. Jiang, and J.J. Steinle. 2019. Epac1 and glycyrrhizin both inhibit HMGB1 levels to reduce diabetes-induced neuronal and vascular damage in the mouse retina. Journal of the Clinical Medicine 8. Liu, L., Y. Jiang, and J.J. Steinle. 2019. Epac1 and glycyrrhizin both inhibit HMGB1 levels to reduce diabetes-induced neuronal and vascular damage in the mouse retina. Journal of the Clinical Medicine 8.
81.
Zurück zum Zitat Luo, F., A. Das, J. Chen, P. Wu, X. Li, and Z. Fang. 2019. Metformin in patients with and without diabetes: A paradigm shift in cardiovascular disease management. Cardiovascular Diabetology 18: 54.PubMedPubMedCentralCrossRef Luo, F., A. Das, J. Chen, P. Wu, X. Li, and Z. Fang. 2019. Metformin in patients with and without diabetes: A paradigm shift in cardiovascular disease management. Cardiovascular Diabetology 18: 54.PubMedPubMedCentralCrossRef
82.
Zurück zum Zitat Tsoyi, K., H.J. Jang, I.T. Nizamutdinova, Y.M. Kim, Y.S. Lee, H.J. Kim, et al. 2011. Metformin inhibits HMGB1 release in LPS-treated RAW 264.7 cells and increases survival rate of endotoxaemic mice. British Journal of the Pharmacology 162:1498–508. Tsoyi, K., H.J. Jang, I.T. Nizamutdinova, Y.M. Kim, Y.S. Lee, H.J. Kim, et al. 2011. Metformin inhibits HMGB1 release in LPS-treated RAW 264.7 cells and increases survival rate of endotoxaemic mice. British Journal of the Pharmacology 162:1498–508.
83.
Zurück zum Zitat Horiuchi, T., N. Sakata, Y. Narumi, T. Kimura, T. Hayashi, K. Nagano, et al. 2017. Metformin directly binds the alarmin HMGB1 and inhibits its proinflammatory activity. Journal of Biological Chemistry 292: 8436–8446.PubMedPubMedCentralCrossRef Horiuchi, T., N. Sakata, Y. Narumi, T. Kimura, T. Hayashi, K. Nagano, et al. 2017. Metformin directly binds the alarmin HMGB1 and inhibits its proinflammatory activity. Journal of Biological Chemistry 292: 8436–8446.PubMedPubMedCentralCrossRef
85.
Zurück zum Zitat Zhang, T., X. Hu, Y. Cai, B. Yi, and Z. Wen. 2014. Metformin protects against hyperglycemia-induced cardiomyocytes injury by inhibiting the expressions of receptor for advanced glycation end products and high mobility group box 1 protein. Molecular Biology Reports 41: 1335–1340.PubMedCrossRef Zhang, T., X. Hu, Y. Cai, B. Yi, and Z. Wen. 2014. Metformin protects against hyperglycemia-induced cardiomyocytes injury by inhibiting the expressions of receptor for advanced glycation end products and high mobility group box 1 protein. Molecular Biology Reports 41: 1335–1340.PubMedCrossRef
86.
Zurück zum Zitat Mollica, L., F. De Marchis, A. Spitaleri, C. Dallacosta, D. Pennacchini, M. Zamai, et al. 2007. Glycyrrhizin binds to high-mobility group box 1 protein and inhibits its cytokine activities. Chemistry & Biology 14: 431–441.CrossRef Mollica, L., F. De Marchis, A. Spitaleri, C. Dallacosta, D. Pennacchini, M. Zamai, et al. 2007. Glycyrrhizin binds to high-mobility group box 1 protein and inhibits its cytokine activities. Chemistry & Biology 14: 431–441.CrossRef
87.
Zurück zum Zitat Gong, G., L. Xiang, L. Yuan, L. Hu, W. Wu, L. Cai, et al. 2014. Protective effect of glycyrrhizin, a direct HMGB1 inhibitor, on focal cerebral ischemia/reperfusion-induced inflammation, oxidative stress, and apoptosis in rats. PLoS One 9:e89450. Gong, G., L. Xiang, L. Yuan, L. Hu, W. Wu, L. Cai, et al. 2014. Protective effect of glycyrrhizin, a direct HMGB1 inhibitor, on focal cerebral ischemia/reperfusion-induced inflammation, oxidative stress, and apoptosis in rats. PLoS One 9:e89450.
88.
Zurück zum Zitat Mohammad, G., M.M. Siddiquei, A. Othman, M. Al-Shabrawey, and A.M. Abu El-Asrar. 2013. High-mobility group box-1 protein activates inflammatory signaling pathway components and disrupts retinal vascular-barrier in the diabetic retina. Experimental Eye Research 107: 101–109.PubMedCrossRef Mohammad, G., M.M. Siddiquei, A. Othman, M. Al-Shabrawey, and A.M. Abu El-Asrar. 2013. High-mobility group box-1 protein activates inflammatory signaling pathway components and disrupts retinal vascular-barrier in the diabetic retina. Experimental Eye Research 107: 101–109.PubMedCrossRef
89.
Zurück zum Zitat Abu El-Asrar, A.M., M.M. Siddiquei, M.I. Nawaz, K. Geboes, and G. Mohammad. 2014. The proinflammatory cytokine high-mobility group box-1 mediates retinal neuropathy induced by diabetes. Mediators of Inflammation 2014:746415. Abu El-Asrar, A.M., M.M. Siddiquei, M.I. Nawaz, K. Geboes, and G. Mohammad. 2014. The proinflammatory cytokine high-mobility group box-1 mediates retinal neuropathy induced by diabetes. Mediators of Inflammation 2014:746415.
90.
Zurück zum Zitat Dandona, P., H. Ghanim, K. Green, C.L. Sia, S. Abuaysheh, N. Kuhadiya, et al. 2013. Insulin infusion suppresses while glucose infusion induces Toll-like receptors and high-mobility group-B1 protein expression in mononuclear cells of type 1 diabetes patients. American Journal of Physiology, Endocrinology and Metabolism 304: E810–E818.PubMedCrossRef Dandona, P., H. Ghanim, K. Green, C.L. Sia, S. Abuaysheh, N. Kuhadiya, et al. 2013. Insulin infusion suppresses while glucose infusion induces Toll-like receptors and high-mobility group-B1 protein expression in mononuclear cells of type 1 diabetes patients. American Journal of Physiology, Endocrinology and Metabolism 304: E810–E818.PubMedCrossRef
91.
Zurück zum Zitat Delucchi, F., R. Berni, C. Frati, S. Cavalli, G. Graiani, R. Sala, et al. Resveratrol treatment reduces cardiac progenitor cell dysfunction and prevents morpho-functional ventricular remodeling in type-1 diabetic rats. PLoS One 7:e39836. Delucchi, F., R. Berni, C. Frati, S. Cavalli, G. Graiani, R. Sala, et al. Resveratrol treatment reduces cardiac progenitor cell dysfunction and prevents morpho-functional ventricular remodeling in type-1 diabetic rats. PLoS One 7:e39836.
92.
Zurück zum Zitat Wu, H., Z. Chen, J. Xie, L.N. Kang, L. Wang, and B. Xu. 2016. High Mobility Group Box-1: A missing link between diabetes and its complications. Mediators of Inflammation 2016: 3896147.PubMedPubMedCentral Wu, H., Z. Chen, J. Xie, L.N. Kang, L. Wang, and B. Xu. 2016. High Mobility Group Box-1: A missing link between diabetes and its complications. Mediators of Inflammation 2016: 3896147.PubMedPubMedCentral
93.
Zurück zum Zitat Diao, H., Z. Kang, F. Han, and W. Jiang. 2014. Astilbin protects diabetic rat heart against ischemia-reperfusion injury via blockade of HMGB1-dependent NF-κB signaling pathway. Food and Chemical Toxicology 63: 104–110.PubMedCrossRef Diao, H., Z. Kang, F. Han, and W. Jiang. 2014. Astilbin protects diabetic rat heart against ischemia-reperfusion injury via blockade of HMGB1-dependent NF-κB signaling pathway. Food and Chemical Toxicology 63: 104–110.PubMedCrossRef
94.
Zurück zum Zitat Kikuchi, K., S. Tancharoen, T. Ito, Y. Morimoto-Yamashita, N. Miura, K. Kawahara, et al. 2013. Potential of the angiotensin receptor blockers (ARBs) telmisartan, irbesartan, and candesartan for inhibiting the HMGB1/RAGE axis in prevention and acute treatment of stroke. International Journal of Molecular Sciences 14: 18899–18924.PubMedPubMedCentralCrossRef Kikuchi, K., S. Tancharoen, T. Ito, Y. Morimoto-Yamashita, N. Miura, K. Kawahara, et al. 2013. Potential of the angiotensin receptor blockers (ARBs) telmisartan, irbesartan, and candesartan for inhibiting the HMGB1/RAGE axis in prevention and acute treatment of stroke. International Journal of Molecular Sciences 14: 18899–18924.PubMedPubMedCentralCrossRef
Metadaten
Titel
Role of High Mobility Group Box 1 in Cardiovascular Diseases
verfasst von
Souad Belmadani
Khalid Matrougui
Publikationsdatum
07.04.2022
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 5/2022
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-022-01668-3

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