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Effect of a Home-Based Wearable Continuous ECG Monitoring Patch on Detection of Undiagnosed Atrial Fibrillation The mSToPS Randomized Clinical Trial Changes in high-sensitivity troponin after drug-coated balloon angioplasty for drug-eluting stent restenosis sST2 Predicts Outcome in Chronic Heart Failure Beyond NT−proBNP and High-Sensitivity Troponin T Impact of Statins on Cardiovascular Outcomes Following Coronary Artery Calcium Scoring Comparison of Heart Team vs Interventional Cardiologist Recommendations for the Treatment of Patients With Multivessel Coronary Artery Disease In-Hospital Costs and Costs of Complications of Chronic Total Occlusion Angioplasty Insights From the OPEN-CTO Registry Association of CYP2C19 Loss-of-Function Alleles with Major Adverse Cardiovascular Events of Clopidogrel in Stable Coronary Artery Disease Patients Undergoing Percutaneous Coronary Intervention: Meta-analysis Incidence, Predictors, and Outcomes of In-Hospital Percutaneous Coronary Intervention Following Coronary Artery Bypass Grafting Level of Scientific Evidence Underlying the Current American College of Cardiology/American Heart Association Clinical Practice Guidelines Improving the Design of Future PCI Trials for Stable Coronary Artery Disease: JACC State-of-the-Art Review
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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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