CBS 2019
CBSMD教育中心
English

科学研究

科研文章

荐读文献

Drug-Coated Balloon Treatment for Femoropopliteal Artery Disease: The IN.PACT Global Study De Novo In-Stent Restenosis Imaging Cohort Acute Myocardial Injury in Patients Hospitalized With COVID-19 Infection: A Review Thin Composite-Wire-Strut Zotarolimus-Eluting Stents Versus Ultrathin-Strut Sirolimus-Eluting Stents in BIONYX at 2 Years A Randomized Trial Comparing the NeoVas Sirolimus-Eluting Bioresorbable Scaffold and Metallic Everolimus-Eluting Stents Guiding Principles for Chronic Total Occlusion Percutaneous Coronary Intervention Universal Definition of Myocardial Infarction Individualizing Revascularization Strategy for Diabetic Patients With Multivessel Coronary Disease Treatment of higher-risk patients with an indication for revascularization: evolution within the field of contemporary percutaneous coronary intervention Heart Disease and Stroke Statistics-2019 Update: A Report From the American Heart Association Derivation and Validation of a Chronic Total Coronary Occlusion Intervention Procedural Success Score From the 20,000-Patient EuroCTO Registry:The EuroCTO (CASTLE) Score

Review Article2020 Dec 18;105383.

JOURNAL:Pharmacol Res. Article Link

Endoplasmic reticulum stress in doxorubicin-induced cardiotoxicity may be therapeutically targeted by natural and chemical compounds: A review

F Yarmohammadi, R Rezaee, AW Haye et al. Keywords: apoptosis; autophagy; cardiac damage; doxorubicin; inflammation

ABSTRACT

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.