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|本期目录/Table of Contents|

糖尿病性心肌病心肌纤维化治疗的进展

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2015年第2期
页码:
233-236
栏目:
综述
出版日期:
2014-10-25

文章信息/Info

Title:
New therapeutic developments for fibrotic disease in diabetic cardiomyopathy
作者:
李国华1; 2; 张 鹏1; 贾 敏2; 董 玲2
(1.兰州军区乌鲁木齐总医院骨科， 新疆 乌鲁木齐 830000；
2.第四军医大学基础部生理学教研室，陕西 西安 710032)
Author(s):
LI Guo-hua1; 2;  ZHANG Peng1;  JIA Min2;  DONG Ling2
(1.Department of Orthopedics, Urumqi General Hospital, Lanzhou Military Area Command, Urumqi 830000, Xinjiang, China；
2.Depatrment of Physiology, School of Basic Medical Sciences, Fourth Military Medical University, Xi’an 710032, Shaanxi, China)
关键词:
糖尿病; 心肌病; 心肌成纤维细胞; 心肌纤维化
Keywords:
diabetes mellitus;  cardiomyopathy;  cardiac fibroblasts;  fibrosis
分类号:
R587.2
DOI:
-
文献标识码:
A
摘要:
糖尿病性心肌病(DCM)是继发于糖尿病(DM)的一种特异性心肌病，可引发心肌肥大、间质纤维化和心肌细胞凋亡。高血糖、肾素-血管紧张素-醛固酮系统(RAAS)系统、炎性因子和基质金属蛋白酶(MMP)的异常增多等多种因素与其发生机制有关。本文对近年DCM纤维化改变的治疗进展予以综述，以期为临床治疗提供依据。
Abstract:
Diabetic cardiomyopathic changes include cardiac hypertrophy, interstitial fibrosis and apoptosis of cardiomyoctes. Hyperglycemia, renin-angiotensin-aldosterone system (RAAS), inflammatory factors and matrix metalloproteinases are believed to be associated with diabetic cardiac fibrosis disease. This article reviews new therapeutic developments for diabetic myocardial fibrosis.

参考文献/References

[1]Tang M,Zhong M,Shang Y,et al.Differential regulation of collagen types I and III expression in cardiac fibroblasts by AGEs through TRB3/MAPK signaling pathway[J].Cell Mol Life Sci,2008,65(18):2924-2932.
[2]Ma YX,Li WH,Xie Q.Rosuvastatin inhibits TGF-beta1 expression and alleviates myocardial fibrosis in diabetic rats[J].Pharmazie,2013,68(5):355-358.
[3]Kawai T,Masaki T,Doi S,et al.PPAR-gamma agonist attenuates renal interstitial fibrosis and inflammation through reduction of TGF-beta[J].Lab Invest,2009,89(1):47-58.
[4]Zhang W,Wu R,Zhang F,et al.Thiazolidinediones improve hepatic fibrosis in rats with non-alcoholic steatohepatitis by activating the adenosine monophosphate-activated protein kinase signalling pathway[J].Clin Exp Pharmacol Physiol,2012,39(12):1026-1033.
[5]Elrashidy RA,Asker ME,Mohamed HE.Pioglitazone attenuates cardiac fibrosis and hypertrophy in a rat model of diabetic nephropathy[J].J Cardiovasc Pharmacol Ther,2012,17(3):324-333.
[6]Zhao Y,Zhang L,Qiao Y,et al.Heme oxygenase-1 prevents cardiac dysfunction in streptozotocin-diabetic mice by reducing inflammation,oxidative stress,apoptosis and enhancing autophagy[J].PLoS One,2013,8(9):e75927-e75938.
[7]Cao J,Sodhi K,Puri N,et al.High fat diet enhances cardiac abnormalities in SHR rats:Protective role of heme oxygenase-adiponectin axis[J].Diabetol Metab Syndr,2011,3(1):37-62.
[8]Li CJ,Lv L,Li H,et al.Cardiac fibrosis and dysfunction in experimental diabetic cardiomyopathy are ameliorated by alpha-lipoic acid[J].Cardiovasc Diabetol,2012,11:73-82.
[9]Connelly KA,Kelly DJ,Zhang Y,et al.Inhibition of protein kinase C-beta by ruboxistaurin preserves cardiac function and reduces extracellular matrix production in diabetic cardiomyopathy[J].Circ Heart Fail,2009,2(2):129-137.
[10]Pfab T,Hocher B.Tranilast and hypertensive heart disease:further insights into mechanisms of an anti-inflammatory and anti-fibrotic drug[J].J Hypertens,2004,22(5):883-886.
[11]See F,Watanabe M,Kompa AR,et al.Early and delayed tranilast treatment reduces pathological fibrosis following myocardial infarction[J].Heart Lung Circ,2013,22(2):122-132.
[12]Gu HP,Lin S,Xu M,et al.Up-regulating relaxin expression by G-quadruplex interactive ligand to achieve antifibrotic action[J].Endocrinology,2012,153(8):3692-3700.
[13]Samuel CS,Hewitson TD,Zhang Y,et al.Relaxin ameliorates fibrosis in experimental diabetic cardiomyopathy[J].Endocrinology,2008,149(7):3286-3293.
[14]Samuel CS,Hewitson TD,Zhang Y,et al.Relaxin ameliorates fibrosis in experimental diabetic cardiomyopathy[J].Endocrinology,2008,149(7):3286-3293.
[15]Lipson KE,Wong C,Teng Y,et al.CTGF is a central mediator of tissue remodeling and fibrosis and its inhibition can reverse the process of fibrosis[J].Fibrogenesis Tissue Repair,2012,5(Suppl 1):S24-S39.
[16]Xue W,Liu Y,Zhao J,et al.Activation of HIF-1 by metallothionein contributes to cardiac protection in the diabetic heart[J].Am J Physiol Heart Circ Physiol,2012,302(12):H2528-H2535.
[17]Samuel SM,Thirunavukkarasu M,Penumathsa SV,et al.Thioredoxin-1 gene therapy enhances angiogenic signaling and reduces ventricular remodeling in infarcted myocardium of diabetic rats[J].Circulation,2010, 121(10):1244-1255.
[18]Meloni M,Descamps B,Caporali A,et al.Nerve growth factor gene therapy using adeno-associated viral vectors prevents cardiomyopathy in type 1 diabetic mice[J].Diabetes,2012,61(1):229-240.
[19]Duisters RF,Tijsen AJ,Schroen B,et al.miR-133 and miR-30 regulate connective tissue growth factor:implications for a role of microRNAs in myocardial matrix remodeling[J].Circ Res,2009,104(2):170-178,6p-178p.
[20]van Rooij E,Sutherland LB,Thatcher JE,et al.Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis[J].Proc Natl Acad Sci U S A,2008,105(35):13027-13032.
[21]Thum T,Gross C,Fiedler J,et al.MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts[J].Nature,2008,456(7224):980-984.
[22]Bernardo BC,Gao XM,Winbanks CE,et al.Therapeutic inhibition of the miR-34 family attenuates pathological cardiac remodeling and improves heart function[J].Proc Natl Acad Sci U S A,2012,109(43):17615-17620.
[23]Pan Z,Sun X,Shan H,et al.MicroRNA-101 inhibited postinfarct cardiac fibrosis and improved left ventricular compliance via the FBJ osteosarcoma oncogene/transforming growth factor-beta1 pathway[J].Circulation,2012,126(7):840-850.
[24]Glass CE,Singal PK,Singla DK.Stem cells in the diabetic infarcted heart[J].Heart Fail Rev,2010,15(6):581-588.
[25]Zhang N,Li J,Luo R,et al.Bone marrow mesenchymal stem cells induce angiogenesis and attenuate the remodeling of diabetic cardiomyopathy[J].Exp Clin Endocrinol Diabetes,2008,116(2):104-111.
[26]Neel S,Singla DK.Induced pluripotent stem(iPS)cells inhibit apoptosis and fibrosis in streptozotocin-induced diabetic rats[J].Mol Pharm,2011, 8(6):2350-2357.

备注/Memo

备注/Memo:
收稿日期：2014-04-14.
基金项目：国家自然科学基金资助（81470412）；国家科技重大专项目资助(2009ZX09301-009)；陕西省中医管理局中医药科研项目资助(jc 38)
通讯作者：张鹏，主治医师，主要从事干细胞与组织工程研究 Email：zhang709@fmmu.edu.cn
作者简介：李国华，本科生 Email：liguohua@fmmu.edu.cn
更新日期/Last Update: 2014-11-18