糖尿病肾病中足突细胞自噬机制的研究进展
摘要
目的糖尿病肾病(DN)是糖尿病的常见并发症。肾脏足突细胞损伤、凋亡及自噬均参与了DN的发生发展过程。其中自噬作为一种溶酶体降解途径,可以通过各条途径被激活从而维持细胞稳态,提示自噬可能成为治疗DN的新靶点。本文主要就近年来DN中足突细胞自噬机制的研究进展进行综述。
引文
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[27]YADAV A,VALLABU S,ARORA S,et al.ANGⅡpromotes autophagy in podocytes[J].American Journal of Physiology-Cell Physiology,2010,299(2):C488-C496.
[28]THARAUX P L,HUBER T B.How many ways can a podocyte die[J]?Seminars in Nephrology,2012,32(4):394-404.
[29]OLTEAN S,QIU Y,FERGUSON J K,et al.Vascular endothelial growth factor-A165bis protective and restores endothelial glycocalyx in diabetic nephropathy[J].Journal of the American Society of Nephrology,2015,26(8):1889-1904.
[30]SHEN Weili,TIAN Chuan,CHEN Hong,et al.Oxidative stress mediates chemerin-induced autophagy in endothelial cells[J].Free Radical Biology and Medicine,2013,55:73-82.
[31]WEI Miaomiao,LIU Chunhua,ZHANG Xiaochen,et al.Autophagy is involved in regulating VEGF during high-glucoseinduced podocyte injury[J].Molecular Biosystems,2016,12(7):2202-2212.
[32]YANG S Y,KIM N H,CHO Y S,et al.Convallatoxin,a dual inducer of autophagy and apoptosis,inhibits angiogenesis in vitro and in vivo[J].PLoS One,2014,9(3):e91094.
[2]MALAVIYA R,LASKIN J D,LASKIN D L.Oxidative stress-induced autophagy:role in pulmonary toxicity[J].Toxicology and Applied Pharmacology,2014,275(2):145-151.
[3]MIZUSHIMA N,KOMATSU M.Autophagy:renovation of cells and tissues[J].Cell,2011,147(4):728-741.
[4]YAMAHARA K,YASUDA M,KUME S,et al.The role of autophagy in the pathogenesis of diabetic nephropathy[J].Journal of Diabetes Research,2013,2013:193757.
[5]LIU L P,WISE D R,DIEHL J A,et al.Hypoxic reactive oxygen species regulate the integrated stress response and cell survival[J].Journal of Biological Chemistry,2008,283(45):31153-31162.
[6]CHEN J C,CHEN M X,FOGO A B,et al.mVps34deletion in podocytes causes glomerulosclerosis by disrupting intracellular vesicle trafficking[J].Journal of the American Society of Nephrology,2013,24(2):198-207.
[7]KUME S,THOMAS M C,KOYA D.Nutrient sensing,autophagy,and diabetic nephropathy[J].Diabetes,2012,61(1):23-29.
[8]LENOIR O,JASIEK M,HENIQUE C,et al.Endothelial cell and podocyte autophagy synergistically protect from diabetesinduced glomerulosclerosis[J].Autophagy,2015,11(7):1130-1145.
[9]TAGAWA A,YASUDA M,KUME S,et al.Impaired podocyte autophagy exacerbates proteinuria in diabetic nephropathy[J].Diabetes,2016,65(3):755-767.
[10]LIU J,LI Q X,WANG X J,et al.β-Arrestins promote podocyte injury by inhibition of autophagy in diabetic nephropathy[J].Cell Death&Disease,2016,7:e2183.
[11]BOYA P,REGGIORI F,CODOGNO P.Emerging regulation and functions of autophagy[J].Nature Cell Biology,2013,15(7):713-720.
[12]HOSOKAWA N,HARA T,KAIZUKA T,et al.Nutrientdependent mTORC1association with the ULK1-Atg13-FIP200complex required for autophagy[J].Molecular Biology of the Cell,2009,20(7):1981-1991.
[13]HOYER-HANSEN M,JAATTELA M.AMP-activated protein kinase:a universal regulator of autophagy[J]?Autophagy,2007,3(4):381-383.
[14]LEE I H,CAO L,MOSTOSLAVSKY R,et al.A role for the NAD-dependent deacetylase Sirt1in the regulation of autophagy[J].Proceedings of the National Academy of Sciences of the United States of America,2008,105(9):3374-3379.
[15]KIM J,KUNDU M,VIOLLET B,et al.AMPK and mTORregulate autophagy through direct phosphorylation of Ulk1[J].Nature Cell Biology,2011,13(2):132-141.
[16]INOKI K,MORI H,WANG J Y,et al.mTORC1activation in podocytes is a critical step in the development of diabetic nephropathy in mice[J].The Journal of Clinical Investigation,2011,121(6):2181-2196.
[17]LAPLANTE M,SABATINI D M.mTOR signaling in growth control and disease[J].Cell,2012,149(2):274-293.
[18]MACK H I,ZHENG B,ASARA J M,et al.AMPK-dependent phosphorylation of ULK1regulates ATG9localization[J].Autophagy,2012,8(8):1197-1214.
[19]JIN Yingli,LIU Shuping,MA Qingshan,et al.Berberine enhances the AMPK activation and autophagy and mitigates high glucose-induced apoptosis of mouse podocytes[J].European Journal of Pharmacology,2017,794:106-114.
[20]LI Dong,LU Zhenyu,XU Zhongwei,et al.Spironolactone promotes autophagy via inhibiting PI3K/AKT/mTOR signalling pathway and reduce adhesive capacity damage in podocytes under mechanical stress[J].Bioscience Reports,2016,36(4):e00355.
[21]POPULO H,LOPES J M,SOARES P.The mTOR signalling pathway in human cancer[J].International Journal of Molecular Sciences,2012,13(2):1886-1918.
[22]ARNS W,BUDDE K,EITNER F,et al.Conversion from a calcineurin inhibitor to a sirolimus-based therapy after renal transplantation-an update of existing recommendations[J].Deutsche Medizinische Wochenschrift,2011,136(49):2554-2559.
[23]MADKE B.Topical rapamycin(sirolimus)for facial angiofibromas[J].Indian Dermatology Online Journal,2013,4(1):54-57.
[24]PARK E Y,PARK J B.High glucose-induced oxidative stress promotes autophagy through mitochondrial damage in rat notochordal cells[J].International Orthopaedics,2013,37(12):2507-2514.
[25]CHEN Haiyang,LUO Zaili,SUN Wen,et al.Low glucose promotes CD133mAb-elicited cell death via inhibition of autophagy in hepatocarcinoma cells[J].Cancer Letters,2013,336(1):204-212.
[26]MA Tean,ZHU Jili,CHEN Xinghua,et al.High glucose induces autophagy in podocytes[J].Experimental Cell Research,2013,319(6):779-789.
[27]YADAV A,VALLABU S,ARORA S,et al.ANGⅡpromotes autophagy in podocytes[J].American Journal of Physiology-Cell Physiology,2010,299(2):C488-C496.
[28]THARAUX P L,HUBER T B.How many ways can a podocyte die[J]?Seminars in Nephrology,2012,32(4):394-404.
[29]OLTEAN S,QIU Y,FERGUSON J K,et al.Vascular endothelial growth factor-A165bis protective and restores endothelial glycocalyx in diabetic nephropathy[J].Journal of the American Society of Nephrology,2015,26(8):1889-1904.
[30]SHEN Weili,TIAN Chuan,CHEN Hong,et al.Oxidative stress mediates chemerin-induced autophagy in endothelial cells[J].Free Radical Biology and Medicine,2013,55:73-82.
[31]WEI Miaomiao,LIU Chunhua,ZHANG Xiaochen,et al.Autophagy is involved in regulating VEGF during high-glucoseinduced podocyte injury[J].Molecular Biosystems,2016,12(7):2202-2212.
[32]YANG S Y,KIM N H,CHO Y S,et al.Convallatoxin,a dual inducer of autophagy and apoptosis,inhibits angiogenesis in vitro and in vivo[J].PLoS One,2014,9(3):e91094.