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Negative Risk Markers for Cardiovascular Events in the Elderly Positive remodeling at 3 year follow up is associated with plaque-free coronary wall segment at baseline: a serial IVUS study Meta-Analysis of Comparison of 5-Year Outcomes of Percutaneous Coronary Intervention Versus Coronary Artery Bypass Grafting in Patients With Unprotected Left Main Coronary Artery in the Era of Drug-eluting Stents Noninvasive Imaging for the Evaluation of Diastolic Function: Promises Fulfilled Long-term results after PCI of unprotected distal left main coronary artery stenosis: the Bifurcations Bad Krozingen (BBK)-Left Main Registry Long-term outcome of prosthesis-patient mismatch after transcatheter aortic valve replacement Usefulness of intravascular ultrasound to predict outcomes in short-length lesions treated with drug-eluting stents Defining a new standard for IVUS optimized drug eluting stent implantation: the PRAVIO study Differential prognostic impact of treatment strategy among patients with left main versus non-left main bifurcation lesions undergoing percutaneous coronary intervention: results from the COBIS (Coronary Bifurcation Stenting) Registry II Regurgitant Volume/Left Ventricular End-Diastolic Volume Ratio: Prognostic Value in Patients With Secondary Mitral Regurgitation
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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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