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Canadian spontaneous coronary artery dissection cohort study: in-hospital and 30-day outcomes Intravenous Statin Administration During Myocardial Infarction Compared With Oral Post-Infarct Administration Coronary CT Angiography and 5-Year Risk of Myocardial Infarction Prevalence of Coronary Vasospasm Using Coronary Reactivity Testing in Patients With Spontaneous Coronary Artery Dissection Pharmacotherapy in the Management of Anxiety and Pain During Acute Coronary Syndromes and the Risk of Developing Symptoms of Posttraumatic Stress Disorder Heart Failure With Preserved, Borderline, and Reduced Ejection Fraction: 5-Year Outcomes Coronary Angiography in Patients With Out-of-Hospital Cardiac Arrest Without ST-Segment Elevation: A Systematic Review and Meta-Analysis Post-Discharge Bleeding and Mortality Following Acute Coronary Syndromes With or Without PCI Transition of Macrophages to Fibroblast-Like Cells in Healing Myocardial Infarction Morphine and Cardiovascular Outcomes Among Patients With Non-ST-Segment Elevation Acute Coronary Syndromes Undergoing Coronary Angiography

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.