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Regional Heterogeneity in the Coronary Vascular Response in Women With Chest Pain and Nonobstructive Coronary Artery Disease Aortic Valve Stenosis Treatment Disparities in the Underserved JACC Council Perspectives 2019 Guidelines on Diabetes, Pre-Diabetes and Cardiovascular Diseases developed in collaboration with the EASD ESC Clinical Practice Guidelines Relationship Between Hospital Surgical Aortic Valve Replacement Volume and Transcatheter Aortic Valve Replacement Outcomes Optimal duration of dual antiplatelet therapy after drug-eluting stent implantation: a randomized, controlled trial. Chimney technique in a TAVR-in-TAVR procedure with high risk of left main artery ostium occlusion Noninvasive Nuclear SPECT Myocardial Blood Flow Quantitation to Guide Management for Coronary Artery Disease Clopidogrel or ticagrelor in acute coronary syndrome patients treated with newer-generation drug-eluting stents: CHANGE DAPT Impact of Intravascular Ultrasound-Guided Drug-Eluting Stent Implantation on Patients With Chronic Kidney Disease: Subgroup Analysis From ULTIMATE Trial Transcatheter versus Surgical Aortic Valve Replacement in Patients with Prior Cardiac Surgery in the Randomized PARTNER 2A Trial
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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.
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