[1]崔方强.足细胞上皮间质转分化研究[J].医学信息,2019,32(22):21-23.[doi:10.3969/j.issn.1006-1959.2019.22.008]
 CUI Fang-qiang.Epithelial Transdifferentiation of Podocytes[J].Journal of Medical Information,2019,32(22):21-23.[doi:10.3969/j.issn.1006-1959.2019.22.008]
点击复制

足细胞上皮间质转分化研究()
分享到:

医学信息[ISSN:1006-1959/CN:61-1278/R]

卷:
32卷
期数:
2019年22期
页码:
21-23
栏目:
综述
出版日期:
2019-11-15

文章信息/Info

Title:
Epithelial Transdifferentiation of Podocytes
文章编号:
1006-1959(2019)22-0021-03
作者:
崔方强
(首都医科大学附属北京中医医院肾病科,北京 100010)
Author(s):
CUI Fang-qiang
(Department of Nephrology,Beijing Traditional Chinese Medicine Hospital,Capital Medical University,Beijing 100010,China)
关键词:
足细胞上皮间质转分化信号通路慢性肾脏病
Keywords:
PodocytesEpithelial-mesenchymal transitionSignaling pathwayChronic kidney disease
分类号:
R692
DOI:
10.3969/j.issn.1006-1959.2019.22.008
文献标志码:
A
摘要:
足细胞是肾小球滤过膜的重要组成部分,在维持肾小球正常滤过功能方面起着至关重要的作用。足细胞上皮间质转分化(EMT)是多种慢性肾脏疾病蛋白尿产生及疾病进展的重要病理机制。减轻足细胞EMT已经成为慢性肾脏疾病防治研究的热点。基于此,本文主要就足细胞的生理特点、EMT病理过程及相关信号通路作一综述。
Abstract:
Podocytes are an important component of glomerular filtration membrane and play a vital role in maintaining normal glomerular filtration function. Epithelial mesenchymal transition (EMT) of podocytes is an important pathological mechanism for proteinuria production and disease progression in a variety of chronic kidney diseases. Reducing podocyte EMT has become a hot spot in the prevention and treatment of chronic kidney disease. Based on this, this paper reviews the physiological characteristics of podocytes, pathological processes of EMT and related signaling pathways.

参考文献/References:

[1]Assady S,Wanner N,Skorecki KL,et al.New Insights into Podocyte Biology in Glomerular Health and Disease[J].J Am Soc Nephrol,2017,28(6):1707-1715. [2]Nagata M.Podocyte injury and its consequences[J].Kidney Int,2016,89(6):1221-1230. [3]Bose M,Almas S,Prabhakar S.Wnt signaling and podocyte dysfunction in diabetic nephropathy[J].J Investig Med,2017,65(8):1093-1101. [4]Sakhi H,Moktefi A,Bouachi K,et al.Podocyte Injury in Lupus Nephritis[J].J Clin Med,2019,8(9):1340. [5]Yoshimura Y,Nishinakamura R.Podocyte development, disease, and stem cell research[J].Kidney Int,2019(19):590-593. [6]Torban E,Braun F,Wanner N,et al.From podocyte biology to novel cures for glomerular disease[J].Kidney Int,2019(19):583-589. [7]Lu CC,Wang GH,Lu J,et al.Role of Podocyte Injury in Glomerulosclerosis[J].Adv Exp Med Biol,2019(1165):195-232. [8]Szrejder M,Piwkowska A.AMPK signalling:Implications for podocyte biology in diabetic nephropathy[J].Biol Cell,2019,111(5):109-120. [9]Chebotareva NV,Bobkova IN,Lysenko LV.The role of podocytes dysfunction in chronic glomerulonephritis progression[J].Ter Arkh,2018,90(6):92-97. [10]Doublier S,Salvidio G,Lupia E,et al.Nephrin expression is reduced in human diabetic nephropathy: evidence for a distinct role for glycated albumin and angiotensinⅡ[J].Diabetes,2003,52(4):1023-1030. [11]Jin J,Gong J,Zhao L,et al.Inhibition of high mobility group box 1 (HMGB1) attenuates podocyte apoptosis and epithelial-mesenchymal transition by regulating autophagy flux[J].J Diabetes,2019,11(10):826-836. [12]Wang X,Gao Y,Tian N,et al.Astragaloside IV inhibits glucose-induced epithelial-mesenchymal transition of podocytes through autophagy enhancement via the SIRT-NF-κB p65 axis[J].Sci Rep,2019,9(1):323. [13]Ling L,Chen L,Zhang C,et al.High glucose induces podocyte epithelial to mesenchymal transition by demethylation mediated enhancement of MMP9 expression[J].Mol Med Rep,2018,17(4):5642-5651. [14]Fuchshofer R,Ullmann S,Zeilbeck LF,et al.Connective tissue growth factor modulates podocyte actin cytoskeleton and extracellular matrix synthesis and is induced in podocytes upon injury[J].Histochem Cell Biol,2011,136(3):301-319. [15]Perysinaki GS,Moysiadis DK,Bertsias G,et al.Podocyte mainslit diaphragm proteins nephrin and podocin, are affected at early stages of lupus nephritis and correlate with disease histology[J].Lupus,2011,20(8):781-791. [16]Chang YP,Sun B,Han Z,et al.Saxagliptin Attenuates Albuminuria by Inhibiting Podocyte Epithelial- to-Mesenchymal Transition via SDF-1α in Diabetic Nephropathy[J]. Front Pharmacol,2017(8):780. [17]Gui T,Sun Y,Shimokado A,et al.The Roles of Mitogen -Activated Protein Kinase Pathways in TGF -beta -Induced Epithelial -Mesenchymal Transition[J].J Signal Transduct,2012(2012):289243. [18]李静,柳斌,樊均明.TGF-β在足细胞生理功能及病理损伤中的作用[J].中国中西医结合肾病杂志,2011,12(12):1120-1122. [19]Gil D,Ciolczyk-Wierzbicka D,Dulinska-Litewka J,et al.Themechanism of contribution of integrin linked kinase (ILK) to epithelial-mesenchymal transition (EMT)[J].Adv Enzyme Regul,2011,51(1):195-207. [20]Lin CL,Wang JY,et al.Wnt/β-catenin signaling modulates survival of high glucose-stressed mesangial cells[J].Journal of the American.society of Nephrology,2006,17(10):2812-2820. [21]Wu X,Gao Y,Xu L,et al.Exosomes from high glucose-treated glomerular endothelial cells trigger the epithelial-mesenchymal transition and dysfunction of podocytes[J].Sci Rep,2017,7(1):9371. [22]Zhou T,He X,Cheng R,et al.Implication of dysregulation of the canonical wingless-type MMTV integration site (WNT) pathway in diabetic nephropathy[J].Diabetologia,2012,55(1):255-266. [23]Feng Y,Ren J,Gui Y,et al.Wnt/β-Catenin-Promoted Macrophage Alternative Activation Contributes to Kidney Fibrosis[J].J Am Soc Nephrol,2018,29(1):182-193. [24]Shi G,Wu W,Wan YG,et al.Low dose of triptolide ameliorates podocyte epithelial-mesenchymal transition induced by high dose of D-glucose via inhibiting Wnt3α/β-catenin signaling pathway activation[J].China Journal of Chinese Materia Medica,2018,43(1):139-146. [25]Dai C,Stolz DB,et al.Wnt/beta-catenin signaling promotes podocyte dysfunction and albuminuria[J].J Am Soc Nephrol,2009,20(9):1997-2008.

相似文献/References:

[1]陈 婷,刘金彦.PI3K/Akt/mTOR通路与足细胞自噬在糖尿病肾病肾功能修复中的研究[J].医学信息,2022,35(22):170.[doi:10.3969/j.issn.1006-1959.2022.22.042]
 CHEN Ting,LIU Jin-yan.The study of PI3K/Akt/mTOR Pathway and Podocyte Autophagy in Renal Function Repair of Diabetic Nephropathy[J].Journal of Medical Information,2022,35(22):170.[doi:10.3969/j.issn.1006-1959.2022.22.042]

更新日期/Last Update: 2019-11-15