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Active factor XI is associated with the risk of cardiovascular events in stable coronary artery disease patients Angiographic versus functional severity of coronary artery stenoses in the FAME study fractional flow reserve versus angiography in multivessel evaluation Comparative efficacy of two paclitaxel-coated balloons with different excipient coatings in patients with coronary in-stent restenosis: A pooled analysis of the Intracoronary Stenting and Angiographic Results: Optimizing Treatment of Drug Eluting Stent In-Stent Restenosis 3 and 4 trials EHRA/EAPCI expert consensus statement on catheter-based left atrial appendage occlusion – an update Long-Term Outcomes of Different Two-Stent Techniques With Second-Generation Drug-Eluting Stents for Unprotected Left Main Bifurcation Disease: Insights From the FAILS-2 Study Contemporary prevalence of pulmonary arterial hypertension in adult congenital heart disease following the updated clinical classification New Evidence Supporting a Novel Conceptual Framework for Distinguishing Proportionate and Disproportionate Functional Mitral Regurgitation Left main coronary angioplasty: early and late results of 127 acute and elective procedures A Survey on Coronary Atherosclerotic Plaque Tissue Characterization in Intravascular Optical Coherence Tomography Pulmonary vascular lesions occurring in patients with chronic major vessel thromboembolic pulmonary hypertension
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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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