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Diabetic cardiomyopathy: Role of epidermal growth factor receptor tyrosine kinase.

作者信息

Xu Zheng, Cai Lu

机构信息

Cardiovascular Center at the First Hospital of Jilin University, Changchun, China.

Cardiovascular Center at the First Hospital of Jilin University, Changchun, China.

出版信息

J Mol Cell Cardiol. 2015 Jul;84:10-2. doi: 10.1016/j.yjmcc.2015.04.002. Epub 2015 Apr 10.

DOI:10.1016/j.yjmcc.2015.04.002
PMID:25865396
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5288810/
Abstract
摘要

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本文引用的文献

1
EGFR inhibition protects cardiac damage and remodeling through attenuating oxidative stress in STZ-induced diabetic mouse model.表皮生长因子受体抑制通过减轻 STZ 诱导的糖尿病小鼠模型中的氧化应激来保护心脏损伤和重构。
J Mol Cell Cardiol. 2015 May;82:63-74. doi: 10.1016/j.yjmcc.2015.02.029. Epub 2015 Mar 7.
2
Epidermal growth factor receptor inhibition slows progression of diabetic nephropathy in association with a decrease in endoplasmic reticulum stress and an increase in autophagy.表皮生长因子受体抑制作用可减缓糖尿病肾病的进展，同时伴随着内质网应激的减少和自噬的增加。
Diabetes. 2014 Jun;63(6):2063-72. doi: 10.2337/db13-1279. Epub 2014 Apr 4.
3
Targeting the epidermal growth factor receptor in solid tumors: focus on safety.
针对实体瘤中的表皮生长因子受体：聚焦安全性。
Expert Opin Drug Saf. 2014 May;13(5):535-49. doi: 10.1517/14740338.2014.904283. Epub 2014 Apr 1.
4
Molecular mechanisms of diabetic cardiomyopathy.糖尿病心肌病的分子机制。
Diabetologia. 2014 Apr;57(4):660-71. doi: 10.1007/s00125-014-3171-6. Epub 2014 Jan 30.
5
Diabetic cardiomyopathy: mechanisms and new treatment strategies targeting antioxidant signaling pathways.糖尿病心肌病：抗氧化信号通路为靶点的发病机制和新治疗策略。
Pharmacol Ther. 2014 Jun;142(3):375-415. doi: 10.1016/j.pharmthera.2014.01.003. Epub 2014 Jan 22.
6
Activation of ErbB2 and Downstream Signalling via Rho Kinases and ERK1/2 Contributes to Diabetes-Induced Vascular Dysfunction.通过Rho激酶和ERK1/2激活ErbB2及下游信号传导，导致糖尿病诱导的血管功能障碍。
PLoS One. 2013 Jun 27;8(6):e67813. doi: 10.1371/journal.pone.0067813. Print 2013.
7
EGFR and the complexity of receptor crosstalk in the cardiovascular system.EGFR 与心血管系统中受体串扰的复杂性。
Curr Mol Med. 2013 Jan;13(1):3-12.
8
Activation of EGFR/ERBB2 via pathways involving ERK1/2, P38 MAPK, AKT and FOXO enhances recovery of diabetic hearts from ischemia-reperfusion injury.通过涉及 ERK1/2、P38MAPK、AKT 和 FOXO 的途径激活 EGFR/ERBB2 可增强糖尿病心脏对缺血再灌注损伤的恢复。
PLoS One. 2012;7(6):e39066. doi: 10.1371/journal.pone.0039066. Epub 2012 Jun 13.
9
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