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Myocardial bridging of the left anterior descending coronary artery is associated with reduced myocardial perfusion reserve: a 13N-ammonia PET study Coronary Protection to Prevent Coronary Obstruction During TAVR: A Multicenter International Registry Association of Coronary Artery Calcium With Long-term, Cause-Specific Mortality Among Young Adults 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 Serial intravascular ultrasound analysis of the main and side branches in bifurcation lesions treated with the T-stenting technique Conceptual Framework for Addressing Residual Atherosclerotic Cardiovascular Disease Risk in the Era of Precision Medicine Edoxaban-based versus vitamin K antagonist-based antithrombotic regimen after successful coronary stenting in patients with atrial fibrillation (ENTRUST-AF PCI): a randomised, open-label, phase 3b trial Association of White Matter Hyperintensities and Cardiovascular Disease: The Importance of Microcirculatory Disease A Review of the Role of Breast Arterial Calcification for Cardiovascular Risk Stratification in Women Balloon Aortic Valvuloplasty as a Bridge to Aortic Valve Replacement: A Contemporary Nationwide Perspective
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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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