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Cardiovascular Biomarkers and Imaging in Older Adults: JACC Council Perspectives Considerations for Single-Measurement Risk-Stratification Strategies for Myocardial Infarction Using Cardiac Troponin Assays Society of cardiac angiography and interventions: suggested management of the no-reflow phenomenon in the cardiac catheterization laboratory Complete Revascularization Versus Culprit Lesion Only in Patients With ST-Segment Elevation Myocardial Infarction and Multivessel Disease: A DANAMI-3-PRIMULTI Cardiac Magnetic Resonance Substudy A prospective natural-history study of coronary atherosclerosis Impact of lesion complexity on peri-procedural adverse events and the benefit of potent intravenous platelet adenosine diphosphate receptor inhibition after percutaneous coronary intervention: core laboratory analysis from 10 854 patients from the CHAMPION PHOENIX trial Non-invasive detection of coronary inflammation using computed tomography and prediction of residual cardiovascular risk (the CRISP CT study): a post-hoc analysis of prospective outcome data Myocardial Infarction in Young Women Global Chronic Total Occlusion Crossing Algorithm: JACC State-of-the-Art Review Microthrombi As A Major Cause of Cardiac Injury in COVID-19: A Pathologic Study
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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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