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Multimodality imaging in cardiology: a statement on behalf of the Task Force on Multimodality Imaging of the European Association of Cardiovascular Imaging Comparison of Stenting Versus Bypass Surgery According to the Completeness of Revascularization in Severe Coronary Artery Disease: Patient-Level Pooled Analysis of the SYNTAX, PRECOMBAT, and BEST Trials Effect of Smoking on Outcomes of Primary PCI in Patients With STEMI Advances in Clinical Cardiology 2020: A Summary of Key Clinical Trials Eruptive Calcified Nodules as a Potential Mechanism of Acute Coronary Thrombosis and Sudden Death Intraaortic Balloon Pump in Cardiogenic Shock Complicating Acute Myocardial Infarction: Long-Term 6-Year Outcome of the Randomized IABP-SHOCK II Trial High-Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long-Term Outcomes Randomized comparison of stent strut coverage following angiography- or optical coherence tomography-guided percutaneous coronary intervention Myocardial Inflammation Predicts Remodeling and Neuroinflammation After Myocardial Infarction Restenosis, Stent Thrombosis, and Bleeding Complications - Navigating Between Scylla and Charybdis

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.