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Rotational atherectomy in the subadventitial space to allow safe and successful chronic total occlusion recanalization: Pushing the limit further Use of Risk Assessment Tools to Guide Decision-Making in the Primary Prevention of Atherosclerotic Cardiovascular Disease A Special Report From the American Heart Association and American College of Cardiology Design and rationale for the treatment effects of provisional side branch stenting and DK crush stenting techniques in patients with unprotected distal left main coronary artery bifurcation lesions (DKCRUSH V) Trial Dual Antithrombotic Therapy with Dabigatran after PCI in Atrial Fibrillation Double Kissing Crush Versus Provisional Stenting for Left Main Distal Bifurcation Lesions: DKCRUSH-V Randomized Trial Improvement of Clinical Outcome in Patients With ST-Elevation Myocardial Infarction Between 1999 And 2016 in China : The Prospective, Multicenter Registry MOODY Study Risk of Early Adverse Events After Clopidogrel Discontinuation in Patients Undergoing Short-Term Dual Antiplatelet Therapy: An Individual Participant Data Analysis Revision: prognostic impact of baseline glucose levels in acute myocardial infarction complicated by cardiogenic shock-a substudy of the IABP-SHOCK II-trial Respiratory Syncytial Virus and Associations With Cardiovascular Disease in Adults Prognostic Significance of Complex Ventricular Arrhythmias Complicating ST-Segment Elevation Myocardial Infarction
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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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