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A randomized comparison of Coronary Stents according to Short or Prolonged durations of Dual Antiplatelet Therapy in patients with Acute Coronary Syndromes: a pre-specified analysis of the SMART-DATE trial Evaluation and Management of Aortic Stenosis in Chronic Kidney Disease: A Scientific Statement From the American Heart Association Outcomes of procedural complications in transfemoral transcatheter aortic valve replacement Risk Stratification in PAH Transcatheter Versus Surgical Aortic Valve Replacement in Patients With Rheumatic Aortic Stenosis Optimizing outcomes during left main percutaneous coronary intervention with intravascular ultrasound and fractional flow reserve: the current state of evidence Sotatercept for the Treatment of Pulmonary Arterial Hypertension Access Site and Outcomes for Unprotected Left Main Stem Percutaneous Coronary Intervention: An Analysis of the British Cardiovascular Intervention Society Database CD163+ macrophages promote angiogenesis and vascular permeability accompanied by inflammation in atherosclerosis Coronary Atherosclerotic Precursors of Acute Coronary Syndromes
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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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