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Antibody-Based Ticagrelor Reversal Agent in Healthy Volunteers When, where, and how to target vascular inflammation in the post-CANTOS era? Association Between Depressive Symptoms and Incident Cardiovascular Diseases Ticagrelor versus clopidogrel in elective percutaneous coronary intervention (ALPHEUS): a randomised, open-label, phase 3b trial A prospective, randomized, open-label trial of 6-month versus 12-month dual antiplatelet therapy after drug-eluting stent implantation in ST-elevation myocardial infarction: Rationale and design of the Comparison of 1-month Versus 12-month Dual Antiplatelet Therapy after Implantation of Drug-eluting Stents Guided by either Intravascular Ultrasound or Angiography in Patients with Acute Coronary Syndrome: Rationale and Design of Prospective, Multicenter, Randomized, Controlled IVUS-ACS & ULTIMATE-DAPT trial Prognostic Value of Computed Tomography-Derived Extracellular Volume in TAVR Patients With Low-Flow Low-Gradient Aortic Stenosis Percutaneous coronary intervention versus coronary-artery bypass grafting for severe coronary artery disease Evolocumab for Early Reduction of LDL Cholesterol Levels in Patients With Acute Coronary Syndromes (EVOPACS) Efficacy and Safety of Ticagrelor Monotherapy in Patients Undergoing Multivessel PCI
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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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