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糖尿病及糖尿病肾病中的炎症、氧化应激、细胞凋亡和自噬:启示录四骑士。

Inflammation, oxidative stress, apoptosis, and autophagy in diabetes mellitus and diabetic kidney disease: the Four Horsemen of the Apocalypse.

作者信息

Turkmen Kultigin

机构信息

Division of Nephrology, Department of Internal Medicine, Meram School of Medicine, Necmettin Erbakan University, Konya, Turkey.

出版信息

Int Urol Nephrol. 2017 May;49(5):837-844. doi: 10.1007/s11255-016-1488-4. Epub 2016 Dec 29.

DOI:10.1007/s11255-016-1488-4
PMID:28035619
Abstract

Diabetic kidney disease (DKD) can occur in approximately 30-40% of both type 1 and type 2 diabetic patients. The well-established features of DKD include increased serum glucose levels along with chronic low-grade inflammation, OxS, increased advanced glycation end products, sorbitol accumulation, increased hexosamine, and protein kinase C pathway activation. On the other hand, accumulating evidence suggests that novel pathways including apoptosis and autophagy might also play important roles in the pathogenesis and progression of DKD. In this review, the integrated mechanisms of inflammation, oxidative stress, apoptosis, and autophagy are discussed in the pathogenesis as well as progression of DM and DKD.

摘要

糖尿病肾病(DKD)在1型和2型糖尿病患者中发生率约为30%-40%。DKD已明确的特征包括血清葡萄糖水平升高,同时伴有慢性低度炎症、氧化应激(OxS)、晚期糖基化终产物增加、山梨醇蓄积、己糖胺增加以及蛋白激酶C途径激活。另一方面,越来越多的证据表明,包括细胞凋亡和自噬在内的新途径可能在DKD的发病机制和进展中也发挥重要作用。在本综述中,将讨论炎症、氧化应激、细胞凋亡和自噬在糖尿病(DM)和DKD发病机制及进展中的综合机制。

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Challenging the dogma of mitochondrial reactive oxygen species overproduction in diabetic kidney disease.挑战糖尿病肾病中线粒体活性氧过度产生的教条。
Kidney Int. 2016 Aug;90(2):272-279. doi: 10.1016/j.kint.2016.02.043. Epub 2016 May 20.
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The possible role of interleukin-33 as a new player in the pathogenesis of contrast-induced nephropathy in diabetic rats.白细胞介素-33作为糖尿病大鼠造影剂肾病发病机制新参与者的潜在作用。
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p66shc deficiency attenuates high glucose-induced autophagy dysfunction in Schwann cells.p66shc缺陷减轻了高糖诱导的雪旺细胞自噬功能障碍。
Korean J Physiol Pharmacol. 2025 Jan 1;29(1):57-66. doi: 10.4196/kjpp.24.155. Epub 2024 Oct 31.
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