晚期糖基化终末产物在冠心病发生和发展中的作用研究进展

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[1]	Perrone A, Giovino A, Benny J, et al. Advanced glycation end products (AGEs): biochemistry, signaling, analytical methods, and epigenetic effects[J].Oxid Med Cell Longev, 2020, 2020: 1-18.
[2]	Petrie J R, Guzik T J, Touyz R M. Diabetes, hypertension, and cardiovascular disease: clinical insights and vascular mechanisms[J].Can J Cardiol, 2018, 34(5): 575-584.
[3]	Prasad K. AGE-RAGE stress in the pathophysiology of atrial fibrillation and its treatment[J].Int J Angiol, 2020, 29(2):72-80.
[4]	刘青波,李虹伟.晚期糖基化终末产物与动脉粥样硬化[J]. 中国心血管杂志, 2018, 23(1): 87-91.
[5]	Singh S, Siva B V, Ravichandiran V. Advanced glycation end products: key player of the pathogenesis of atherosclerosis[J]. Glycoconj, 2022, 17:123-129.
[6]	Xiao Z L, Ma L P, Yang D F, et al. Profilin-1 is involved in macroangiopathy induced by advanced glycation end products via vascular remodeling and inflammation [J].World J Diabetes, 2021, 12(11): 1875-1893.
[7]	Moldogazieva N T, Mokhosoev I M, Mel’nikova T I, et al. Oxidative stress and advanced lipoxidation and glycation end products (ALEs and AGEs) in aging and age-related diseases[J]. Oxid Med Cell Longev, 2019, 2019(14): 1-14.
[8]	Matsumoto T, Taguchi K, Kobayashi T. Relationships between advanced glycation end products (AGEs), vasoactive substances, and vascular function [J]. Smooth Muscle Res, 2021, 57(0): 94-107.
[9]	Konst R E, Guzik T J, Kaski J C, et al. The pathogenic role of coronary microvascular dysfunction in the setting of other cardiac or systemic conditions [J].Cardiovasc Res, 2020, 116(4): 817-828.
[10]	Barrett E J, Liu Z, Khamaisi M, et al. Diabetic microvascular disease: an endocrine society scientific statement[J].Clin Endocrinol Metab, 2017, 102(12): 4343-4410.
[11]	Liu Z, Zhu H, Ma Y, et al. AGEs exacerbates coronary microvascular dysfunction in NoCAD by activating endoplasmic reticulum stress-mediated PERK signaling pathway [J].Metabolism, 2021, 117: 154710.
[12]	Fishman S L, Sonmez H, Basman C, et al. The role of advanced glycation end-products in the development of coronary artery disease in patients with and without diabetes mellitus: a review [J].Mol Med, 2018, 24(1): 59.
[13]	Bayarsaikhan D, Bayarsaikhan G, Lee B. AGE-RAGE system and its application in stem cell therapy[J]. Stem Cell Res, 2021, 7: 60.
[14]	Raposeiras-Roubín S, Rodino-Janeiro B K, Paradela-Dobarro B, et al. Advanced glycation end-products as long-term predictors of death and reinfarction after an acute coronary syndrome [J].Biomark Med, 2015, 9(3): 209-216.
[15]	Dozio E, Massaccesi L, Corsi Romanelli M M. Glycation and glycosylation in cardiovascular remodeling: focus on advanced glycation end products and O-linked glycosylations as glucose-related pathogenetic factors and disease markers[J].Clin Med, 2021, 10(20): 4792.
[16]	Tsoporis J N, Izhar S, Proteau G, et al. S100B-RAGE dependent VEGF secretion by cardiac myocytes induces myofibroblast proliferation [J]. Mol Cell Cardiol, 2012, 52: 464-473.
[17]	Blackburn N J R, Vulesevic B, McNeill B, et al. Methylglyoxal-derived advanced glycation end products contribute to negative cardiac remodeling and dysfunction post-myocardial infarction[J].Basic Res Cardiol, 2017, 112(5): 57.
[18]	Grauen L H, Yndigegn T, Marinkovic G, et al. The soluble receptor for advanced glycation end-products (sRAGE) has a dual phase-dependent association with residual cardiovascular risk after an acute coronary event [J]. Atherosclerosis, 2019, 287: 16-23.
[19]	Liu Z, Zhang Y, Pan S, et al. Activation of RAGE-dependent endoplasmic reticulum stress associates with exacerbated postmyocardial infarction ventricular arrhythmias in diabetes [J].Am J Physiol Endocrinol Metab, 2021, 320(3): 539-550.
[20]	Evens L, Beliën H, Deluyker D, et al. The impact of advanced glycation end-products (AGEs) on proliferation and apoptosis of primary stem cells: a systematic review[J].Stem Cells Int, 2020, 2020: 1-13.
[21]	Evens L, Heeren E, Rummens J L, et al. Advanced glycation end products impair cardiac atrial appendage stem cells properties[J].Clin Med, 2021, 10(13): 2964.
[22]	Wang X, Wang J, Tu T, et al. Remote ischemic postconditioning protects against myocardial ischemia-reperfusion injury by inhibition of the RAGE-HMGB1 pathway[J].Biomed Res Int, 2018, 2018: 1-9.
[23]	Jensen L J, Flyvbjerg A, Bjerre M. Soluble receptor for advanced glycation end product: a biomarker for acute coronary syndrome[J].Biomed Res Int, 2015, 2015: 1-7.
[24]	Cao X, Li B, Han X, et al. Soluble receptor for advanced glycation end-products promotes angiogenesis through activation of STAT3 in myocardial ischemia/reperfusion injury [J].Apoptosis, 2020, 25(5-6): 341-353.
[25]	Jiang X, Guo C X, Zeng X J, et al. A soluble receptor for advanced glycation end-products inhibits myocardial apoptosis induced by ischemia/reperfusion via the JAK2/STAT3 pathway [J].Apoptosis, 2015, 20(8): 1033-1047.
[26]	Guo C X, Jiang X, Zeng X J, et al. Soluble receptor for advanced glycation end-products protects against ischemia/reperfusion-induced myocardial apoptosis via regulating the ubiquitin proteasome system [J].Free Radic Biol Med, 2016, 94: 17-26.
[27]	Dang M, Zeng X, Chen B, et al. Interferon-γ mediates the protective effects of soluble receptor for advanced glycation end-product in myocardial ischemia reperfusion[J]. Lab Invest, 2019, 99(3): 358-370.
[28]	赵航,王通宇,胡巍娜,等. 晚期糖基化终末产物与心力衰竭的相关性及靶向药物治疗[J].中国老年学杂志, 2021, 41(8): 1780-1784.
[29]	Deluyker D, Evens L, Beliën H, et al. Acute exposure to glycated proteins reduces cardiomyocyte contractile capacity[J]. Exp Physiol, 2019, 104(7): 997-1003.
[30]	Altomare A, Baron G, Balbinot M, et al. In-Depth AGE and ALE profiling of human albumin in heart failure: ex vivo studies[J].Antioxidants (Basel), 2021, 10(3): 358.
[31]	Raposeiras-Roubín S, Rodio-Janeiro B K, Paradela-Dobarro B, et al. Predictive value of advanced glycation end products for the development of post-infarction heart failure: a preliminary report [J].Cardiovasc Diabetol, 2012, 11: 102.
[32]	Sourris K C, Watson A, Jandeleit-Dahm K. Inhibitors of advanced glycation end product (AGE) formation and accumulation[J].Handb Exp Pharmacol, 2021, 264: 395-423.
[33]	Watson A M, Soro-Paavonen A, Sheehy K, et al. Delayed intervention with AGE inhibitors attenuates the progression of diabetes-accelerated atherosclerosis in diabetic apolipoprotein E knockout mice[J].Diabetologia, 2011, 54(3): 681-689.
[34]	Bongarzone S, Savickas V, Luzi F, et.al. Targeting the receptor for advanced glycation endproducts (RAGE): a medicinal chemistry perspective[J]. Med Chem, 2017, 60(17): 7213-7232.
[35]	Deane R, Singh I, Sagare A P, et al. A multimodal RAGE-specific inhibitor reduces amyloid β-mediated brain disorder in a mouse model of Alzheimer disease[J]. Clin Invest, 2012, 122(4): 1377-1392.
[36]	Shen C, Ma Y, Zeng Z, et al. RAGE-specific inhibitor FPS-ZM1 attenuates AGEs-induced neuroinflammation and oxidative stress in rat primary microglia[J].Neurochem Res, 2017, 42(10): 2902-2911.
[37]	Vlad A, Vlad M, Petrica L, et al. Therapy with atorvastatin versus rosuvastatin reduces urinary podocytes, podocyte-associated molecules, and proximal tubule dysfunction biomarkers in patients with type 2 diabetes mellitus: a pilot study[J].Ren Fail, 2017, 39(1): 112-119.

[1]	. [J]. Med. J. Chin. Peop. Armed Poli. Forc., 2020, 31(8): 724-726.