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The impact of intravascular ultrasound guidance during drug eluting stent implantation on angiographic outcomes The conductive function of biopolymer corrects myocardial scar conduction blockage and resynchronizes contraction to prevent heart failure Transcatheter Aortic Valve Replacement vs Surgical Replacement in Patients With Pure Aortic Insufficiency The Role of the Pericardium in Heart Failure: Implications for Pathophysiology and Treatment Three vs twelve months of dual antiplatelet therapy after zotarolimus-eluting stents: the OPTIMIZE randomized trial Long-term effects of intensive glucose lowering on cardiovascular outcomes Incidence, predictors, and outcomes associated with acute kidney injury in patients undergoing transcatheter aortic valve replacement: from the BRAVO-3 randomized trial Percutaneous Left Atrial Appendage Closure for Stroke Prophylaxis in Patients With Atrial Fibrillation: 2.3-Year Follow-up of the PROTECT AF (Watchman Left Atrial Appendage System for Embolic Protection in Patients With Atrial Fibrillation) Trial INTERMACS Profiles and Outcomes Among Non–Inotrope-Dependent Outpatients With Heart Failure and Reduced Ejection Fraction ACC/AHA Versus ESC Guidelines on Dual Antiplatelet Therapy JACC Guideline Comparison: JACC State-of-the-Art Review
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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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