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Single-Molecule hsTnI and Short-Term Risk in Stable Patients With Chest Pain Efficacy and safety of rosuvastatin vs. atorvastatin in lowering LDL cholesterol : A meta-analysis of trials with East Asian populations A VOYAGER Meta-Analysis of the Impact of Statin Therapy on Low-Density Lipoprotein Cholesterol and Triglyceride Levels in Patients With Hypertriglyceridemia Development and validation of a simple risk score to predict 30-day readmission after percutaneous coronary intervention in a cohort of medicare patients 2-Year Outcomes After Stenting of Lipid-Rich and Nonrich Coronary Plaques Cardiac monocytes and macrophages after myocardial infarction Cardiac Troponin Elevation in Patients Without a Specific Diagnosis Successful catheter ablation of electrical storm after myocardial infarction Overall and Cause-Specific Mortality in Randomized Clinical Trials Comparing Percutaneous Interventions With Coronary Bypass Surgery: A Meta-analysis Optimal Stenting Technique for Complex Coronary Lesions Intracoronary Imaging-Guided Pre-Dilation, Stent Sizing, and Post-Dilation
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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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