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Epinephrine Versus Norepinephrine for Cardiogenic Shock After Acute Myocardial Infarction Myocardial infarction with non-obstructive coronary arteries as compared with myocardial infarction and obstructive coronary disease: outcomes in a Medicare population Prevalence of anginal symptoms and myocardial ischemia and their effect on clinical outcomes in outpatients with stable coronary artery disease: data from the International Observational CLARIFY Registry 4-Step Protocol for Disparities in STEMI Care and Outcomes in Women Use of Mechanical Circulatory Support Devices Among Patients With Acute Myocardial Infarction Complicated by Cardiogenic Shock Cardiopulmonary Exercise Testing: What Is its Value? Improved Outcomes Associated with the use of Shock Protocols: Updates from the National Cardiogenic Shock Initiative Chronic total occlusion intervention of the non-infarct-related artery in acute myocardial infarction patients: the Korean multicenter chronic total occlusion registry Heart Regeneration by Endogenous Stem Cells and Cardiomyocyte Proliferation: Controversy, Fallacy, and Progress A Test in Context: E/A and E/e' to Assess Diastolic Dysfunction and LV Filling Pressure
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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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