内质网
心脏毒性
自噬
未折叠蛋白反应
阿霉素
心力衰竭
ULK1
切碎
ASK1
药理学
化学
炎症
医学
细胞凋亡
癌症研究
细胞生物学
激酶
内科学
蛋白激酶A
化疗
生物
生物化学
安普克
丝裂原活化蛋白激酶激酶
作者
Fatemeh Yarmohammadi,Ramin Rezaee,Abdul Haye,Gholamreza Karimi
标识
DOI:10.1016/j.phrs.2020.105383
摘要
Doxorubicin (DOX) is a chemotherapeutic agent with marked, dose-dependent cardiotoxicity that leads to tachycardia, atrial and ventricular arrhythmia, and irreversible heart failure. Induction of the endoplasmic reticulum (ER) which plays a major role in protein folding and calcium homeostasis was reported as a key contributor to cardiac complications of DOX. This article reviews several chemical compounds that have been shown to regulate DOX-induced inflammation, apoptosis, and autophagy via inhibition of ER stress signaling pathways, such as the IRE1α/ASK1/JNK, IRE1α/JNK/Beclin-1, and CHOP pathways.
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