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Successful Treatment of Unprotected Left Main Coronary Bifurcation Lesion Using Minimum Contrast Volume with Intravascular Ultrasound Guidance Astro-CHARM, the First 10-year ASCVD Risk Estimator Incorporating Coronary Calcium Improving the Use of Primary Prevention Implantable Cardioverter-Defibrillators Therapy With Validated Patient-Centric Risk Estimates Mortality Following Cardiovascular and Bleeding Events Occurring Beyond 1 Year After Coronary Stenting - A Secondary Analysis of the Dual Antiplatelet Therapy (DAPT) Study Benefit of switching dual antiplatelet therapy after acute coronary syndrome: the TOPIC (timing of platelet inhibition after acute coronary syndrome) randomized study Intravascular ultrasound guidance in drug-eluting stents implantation: a meta-analysis and trial sequential analysis of randomized controlled trials Relationship Between Infarct Size and Outcomes Following Primary PCI: Patient-Level Analysis From 10 Randomized Trials Intracoronary Optical Coherence Tomography 2018: Current Status and Future Directions Intravascular ultrasound-guided percutaneous coronary intervention in left main coronary bifurcation lesions: a review Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II): final 12 month results of a randomised, open-label trial
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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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