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Two-Year Outcomes and Predictors of Target Lesion Revascularization for Non-Left Main Coronary Bifurcation Lesions Following Two-Stent Strategy With 2nd-Generation Drug-Eluting Stents Complete Revascularization with Multivessel PCI for Myocardial Infarction Appropriate Use Criteria and Health Status Outcomes Following Chronic Total Occlusion Percutaneous Coronary Intervention: Insights From the OPEN-CTO Registry Outcome of Applying the ESC 0/1-hour Algorithm in Patients With Suspected Myocardial Infarction Canadian Multicenter Chronic Total Occlusion Registry: Ten-Year Follow-Up Results of Chronic Total Occlusion Revascularization Five-Year Outcomes after PCI or CABG for Left Main Coronary Disease Efficacy and Safety of Stents in ST-Segment Elevation Myocardial Infarction 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society Randomized Comparison Between Radial and Femoral Large-Bore Access for Complex Percutaneous Coronary Intervention Long-Term Prognostic Implications of Previous Silent Myocardial Infarction in Patients Presenting With Acute Myocardial Infarction

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.