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Management of Myocardial Revascularization Failure: An Expert Consensus Document of the EAPCI Improved outcomes in patients with ST-elevation myocardial infarction during the last 20 years are related to implementation of evidence-based treatments: experiences from the SWEDEHEART registry 1995-2014 Vascular response and healing profile of everolimus-eluting bioresorbable vascular scaffolds for percutaneous treatment of chronic total coronary occlusions: A one-year optical coherence tomography analysis from the GHOST-CTO registry Association of Acute Procedural Results with Long-term Outcomes After CTO-PCI Impact of Optimized Procedure-Related Factors in Drug-Eluting Balloon Angioplasty for Treatment of In-Stent Restenosis Short-term and long-term clinical outcomes of rotational atherectomy in resistant chronic total occlusion Contemporary Diagnosis and Management of Patients With Myocardial Infarction in the Absence of Obstructive Coronary Artery Disease: A Scientific Statement From the American Heart Association Effect of a Restrictive vs Liberal Blood Transfusion Strategy on Major Cardiovascular Events Among Patients With Acute Myocardial Infarction and Anemia: The REALITY Randomized Clinical Trial Clinical Characteristics and Outcomes of STEMI Patients With Cardiogenic Shock and Cardiac Arrest Epidemiology and Clinical Outcomes of Patients With Inflammatory Bowel Disease Presenting With Acute Coronary Syndrome

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.