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mTOR信号通路在糖尿病肾病发病机制中的研究进展 被引量:5

Research Progress of mTOR Pathway in Pathogenesis of Diabetic Nephropathy
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摘要 糖尿病肾病(diabetic nephropathy,DN)是糖尿病最常见的并发症之一,因其具有高发病率且与晚期肾病、心血管疾病和过早死亡等风险相关,糖尿病肾病已成为全球性的公共健康问题,但目前其发病机制尚不清楚。雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)是一种丝氨酸/苏氨酸的蛋白酶,在延迟细胞凋亡以及促进细胞分裂、细胞存活、血管生成中发挥着重要作用。近年来有研究表明,mTOR存在于DN进展的关键步骤中,包括自噬、炎症及氧化应激等。因此,就mTOR介导的自噬、炎症及氧化应激信号通路在DN发病机制中的相关研究进展做一综述,以期为DN治疗及预防提供理论参考。 Diabetic nephropathy(DN)is one of the most common complications of diabetes.Because of its high incidence and related to the risks of advanced kidney disease,cardiovascular disease and premature death,DN has become a global public health problem,but its pathogenesis is still unclear.Mammalian target of rapamycin(mTOR)is a serine/threonine protease,which plays an important role in delaying apoptosis and promoting cell division,cell survival and angiogenesis.Recent studies have shown that mTOR exists in the key steps of DN progression,including autophagy,inflammation and oxidative stress.Therefore,the research progress of mTOR-mediated autophagy,inflammation and oxidative stress signaling pathways in the pathogenesis of DN was reviewed,in order to provide theoretical reference for the treatment and prevention of DN.
作者 王珍 杨洛 廖敏 郝亚荣 WANG Zhen;YANG Luo;LIAO Min;HAO Yarong(Department of Geriatrics,Renmin Hospital of Wuhan University,Wuhan 430060,China)
出处 《生物技术进展》 2021年第3期316-321,共6页 Current Biotechnology
基金 湖北省自然科学基金项目(2016CFB673)。
关键词 糖尿病肾病 雷帕霉素靶蛋白 自噬 炎症反应 氧化应激 diabetic nephropathy mTOR autophagy inflammatory reaction oxidative stress
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  • 1International Diabetes Federation. IDF Diabetes Atlas. 6thed. Brussels, Belgium: International Diabetes Federation, 2013.Available from: URL: http://www.idf.org/diabetesatlas.
  • 2Nolan CJ, Damm P, Prentki M. Type 2 diabetes across generations:from pathophysiology to prevention and management.Lancet 2011; 378: 169-181 [PMID: 21705072 DOI: 10.1016/S0140-6736(11)60614-4].
  • 3Shaw JE, Sicree RA, Zimmet PZ. Global estimates of the prevalenceof diabetes for 2010 and 2030. Diabetes Res Clin Pract 2010; 87: 4-14[PMID: 19896746 DOI: 10.1016/j.diabres.2009.10.007].
  • 4Butler AE, Janson J, Bonner-Weir S, Ritzel R, Rizza RA, ButlerPC. Beta-cell deficit and increased beta-cell apoptosis in humanswith type 2 diabetes. Diabetes 2003; 52: 102-110 [PMID: 12502499DOI: 10.2337/diabetes.52.1.102].
  • 5Ashcroft FM, Rorsman P. Diabetes mellitus and the β cell: thelast ten years. Cell 2012; 148: 1160-1171 [PMID: 22424227 DOI:10.1016/j.cell.2012.02.010].
  • 6Quan W, Jo EK, Lee MS. Role of pancreatic β-cell death andinflammation in diabetes. Diabetes Obes Metab 2013; 15 Suppl 3:141-151 [PMID: 24003931 DOI: 10.1111/dom.12153].
  • 7Brownlee M. Biochemistry and molecular cell biology of diabeticcomplications. Nature 2001; 414: 813-820 [PMID: 11742414 DOI:10.1038/414813a].
  • 8Pickup JC, Crook MA. Is type II diabetes mellitus a disease of theinnate immune system- Diabetologia 1998; 41: 1241-1248 [PMID:9794114 DOI: 10.1007/s001250051058].
  • 9Shoelson SE, Lee J, Goldfine AB. Inflammation and insulinresistance. J Clin Invest 2006; 116: 1793-1801 [PMID: 16823477DOI: 10.1172/JCI29069].
  • 10Donath MY, Dalmas é, Sauter NS, B-ni-Schnetzler M. Inflammationin obesity and diabetes: islet dysfunction and therapeutic opportunity.Cell Metab 2013; 17: 860-872 [PMID: 23747245 DOI: 10.1016/j.cmet.2013.05.001].

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