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SPECT and PET in ischemic heart failure A Fully Magnetically Levitated Circulatory Pump for Advanced Heart Failure The Prevalence of Myocardial Bridging Associated with Coronary Endothelial Dysfunction in Patients with Chest Pain and Non-Obstructive Coronary Artery Disease Meta-analysis of outcomes after intravascular ultrasound-guided versus angiography-guided drug-eluting stent implantation in 26,503 patients enrolled in three randomized trials and 14 observational studies Operator Experience and Outcomes After Left Main Percutaneous Coronary Intervention Universal Definition and Classification of Heart Failure: A Report of the Heart Failure Society of America, Heart Failure Association of the European Society of Cardiology, Japanese Heart Failure Society and Writing Committee of the Universal Definition of Heart Failure Timing of Intervention in Aortic Stenosis Association Between Functional Impairment and Medication Burden in Adults with Heart Failure Baseline Features of the VICTORIA (Vericiguat Global Study in Subjects With Heart Failure With Reduced Ejection Fraction) Trial Angiotensin–Neprilysin Inhibition in Heart Failure with Preserved Ejection Fraction
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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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