Methylglyoxal stimulates endoplasmic reticulum stress in vascular smooth muscle cells

References

• Matheus AS, Tannus LR, Cobas RA, et al. Impact of diabetes on cardiovascular disease: an update. Int J Hypertens. 2013;2013:653789.
   PubMedGoogle Scholar
• Pasquier J, Hoarau-Vechot J, Fakhro K, et al. Epigenetics and cardiovascular disease in diabetes. Curr Diab Rep. 2015;15:108.
   PubMed Web of Science ®Google Scholar
• Rabbani N, Thornalley PJ. Dicarbonyl stress in cell and tissue dysfunction contributing to ageing and disease. Biochem Biophys Res Commun. 2015;458:221–226.
   PubMed Web of Science ®Google Scholar
• Schalkwijk CG. Vascular AGE-ing by methylglyoxal: the past, the present and the future. Diabetologia. 2015;58:1715–1719.
   PubMed Web of Science ®Google Scholar
• Thornalley PJ. Dicarbonyl Intermediates in the Maillard Reaction. Ann N Y Acad Sci. 2005;1043:111–117.
   PubMed Web of Science ®Google Scholar
• Berner AK, Brouwers O, Pringle R, et al. Protection against methylglyoxal-derived AGEs by regulation of glyoxalase 1 prevents retinal neuroglial and vasodegenerative pathology. Diabetologia. 2012;55:845–854.
   PubMed Web of Science ®Google Scholar
• Liu MQ, Chen Z, Chen LX. Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases. Acta Pharmacol Sin. 2016;37:425–443.
   PubMed Web of Science ®Google Scholar
• Zhang K, Kaufman RJ. Protein folding in the endoplasmic reticulum and the unfolded protein response. Handb Exp Pharmacol. 2006:69–91.
   PubMedGoogle Scholar
• Zhou AX, Tabas I. The UPR in atherosclerosis. Semin Immunopathol. 2013;35:321–332.
   PubMed Web of Science ®Google Scholar
• Myoishi M, Hao H, Minamino T, et al. Increased endoplasmic reticulum stress in atherosclerotic plaques associated with acute coronary syndrome. Circulation. 2007;116:1226–1233.
   PubMed Web of Science ®Google Scholar
• Yi N, Chen SY, Ma A, et al. Tunicamycin inhibits PDGF-BB-induced proliferation and migration of vascular smooth muscle cells through induction of HO-1. Anat Rec. 2012;295:1462–1472.
   Google Scholar
• Pedruzzi E, Guichard C, Ollivier V, et al. NAD(P)H oxidase Nox-4 mediates 7-ketocholesterol-induced endoplasmic reticulum stress and apoptosis in human aortic smooth muscle cells. MCB. 2004;24:10703–10717.
   PubMed Web of Science ®Google Scholar
• Zhou J, Werstuck GH, Lhoták Šá, et al. Association of multiple cellular stress pathways with accelerated atherosclerosis in hyperhomocysteinemic apolipoprotein E-deficient mice. Circulation. 2004;110:207–213.
   PubMed Web of Science ®Google Scholar
• Werstuck GH, Khan MI, Femia G, et al. Glucosamine-induced endoplasmic reticulum dysfunction is associated with accelerated atherosclerosis in a hyperglycemic mouse model. Diabetes. 2006;55:93–101.
   PubMed Web of Science ®Google Scholar
• Kirca M, Yesilkaya A. Losartan inhibits EGFR transactivation in vascular smooth muscle cells. Turk J Med Sci. 2018;48:1364–1371.
   PubMed Web of Science ®Google Scholar
• Nowotny K, Castro JP, Hugo M, et al. Oxidants produced by methylglyoxal-modified collagen trigger ER stress and apoptosis in skin fibroblasts. Free Radic Biol Med. 2018;120:102–113.
   PubMed Web of Science ®Google Scholar
• Pei Z, Deng Q, Babcock SA, et al. Inhibition of advanced glycation endproduct (AGE) rescues against streptozotocin-induced diabetic cardiomyopathy: Role of autophagy and ER stress. Toxicol Lett. 2018;284:10–20.
   PubMed Web of Science ®Google Scholar
• Hanssen NMJ, Scheijen JLJM, Jorsal A, et al. Higher plasma methylglyoxal levels are associated with incident cardiovascular disease in individuals with type 1 diabetes: a 12-year follow-up study. Diabetes. 2017;66:2278–2283.
   PubMed Web of Science ®Google Scholar
• Kim S, Kim S, Hwang AR, et al. Apelin-13 inhibits methylglyoxal-induced unfolded protein responses and endothelial dysfunction via regulating AMPK pathway. Int J Mol Sci. 2020;21:4069.
   Web of Science ®Google Scholar
• Liu C, Huang Y, Zhang Y, et al. Intracellular methylglyoxal induces oxidative damage to pancreatic beta cell line INS-1 cell through Ire1α-JNK and mitochondrial apoptotic pathway. Free Radic Res. 2017;51:337–350.
   PubMed Web of Science ®Google Scholar
• Nam DH, Han JH, Kim S, et al. Activated protein C prevents methylglyoxal-induced endoplasmic reticulum stress and cardiomyocyte apoptosis via regulation of the AMP-activated protein kinase signaling pathway. Biochem Biophys Res Commun. 2016;480:622–628.
   PubMed Web of Science ®Google Scholar
• Choi YY, Kim S, Han JH, et al. CHOP deficiency inhibits methylglyoxal-induced endothelial dysfunction. Biochem Biophys Res Commun. 2016;480:362–368.
   PubMed Web of Science ®Google Scholar
• Chan CM, Huang DY, Huang YP, et al. Methylglyoxal induces cell death through endoplasmic reticulum stress-associated ROS production and mitochondrial dysfunction. J Cell Mol Med. 2016;20:1749–1760.
   PubMed Web of Science ®Google Scholar
• Nam DH, Han JH, Lee TJ, et al. CHOP deficiency prevents methylglyoxal-induced myocyte apoptosis and cardiac dysfunction. J Mol Cell Cardiol. 2015;85:168–177.
   PubMed Web of Science ®Google Scholar
• Palsamy P, Bidasee KR, Ayaki M, et al. Methylglyoxal induces endoplasmic reticulum stress and DNA demethylation in the Keap1 promoter of human lens epithelial cells and age-related cataracts. Free Radic Biol Med. 2014;72:134–148.
   PubMed Web of Science ®Google Scholar
• Liu C, Huang Y, Zhang Y, et al. Intracellular methylglyoxal induces oxidative damage to pancreatic beta cell line INS-1 cell through Ire1α-JNK and mitochondrial apoptotic pathway. Free Radical Res. 2017;51:337–350.
   PubMed Web of Science ®Google Scholar
• Lenin R, Mohan V, Balasubramanyam M. SEAP activity serves for demonstrating ER stress induction by glucolipotoxicity as well as testing ER stress inhibitory potential of therapeutic agents. Mol Cell Biochem. 2015;404:271–279.
   PubMed Web of Science ®Google Scholar
• Thornalley PJ. Protein and nucleotide damage by glyoxal and methylglyoxal in physiological systems–role in ageing and disease. Drug Metabol Drug Interact. 2008;23:125–150.
   PubMedGoogle Scholar