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Clinical impact of PCSK9 inhibitor on stabilization and regression of lipid-rich coronary plaques: a near-infrared spectroscopy study Impact of post-intervention minimal stent area on 9-month follow-up patency of paclitaxel-eluting stents: an integrated intravascular ultrasound analysis from the TAXUS IV, V, and VI and TAXUS ATLAS Workhorse, Long Lesion, and Direct Stent Trials Primary Prevention Trial Designs Using Coronary Imaging: A National Heart, Lung, and Blood Institute Workshop Considerations for Optimal Device Selection in Transcatheter Aortic Valve Replacement: A Review Clinical impact of conduction disturbances in transcatheter aortic valve replacement recipients: a systematic review and meta-analysis Percutaneous Coronary Intervention for Vulnerable Coronary Atherosclerotic Plaque Association of Reduced Apical Untwisting With Incident HF in Asymptomatic Patients With HF Risk Factors Why and How to Measure Aortic Valve Calcification in Patients With Aortic Stenosis Intracoronary stenting without anticoagulation accomplished with intravascular ultrasound guidance Contribution of stent underexpansion to recurrence after sirolimus-eluting stent implantation for in-stent restenosis
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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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