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Red Cell Distribution Width in Patients with Diabetes and Myocardial Infarction: an analysis from the EXAMINE trial Clinical and Angiographic Features of Patients With Out-of-Hospital Cardiac Arrest and Acute Myocardial Infarction Mortality in STEMI patients without standard modifiable risk factors: a sex-disaggregated analysis of SWEDEHEART registry data A randomised trial comparing two stent sizing strategies in coronary bifurcation treatment with bioresorbable vascular scaffolds - The Absorb Bifurcation Coronary (ABC) trial Outcomes after drug-coated balloon treatment for patients with calcified coronary lesions A randomised trial comparing two stent sizing strategies in coronary bifurcation treatment with bioresorbable vascular scaffolds - The Absorb Bifurcation Coronary (ABC) trial Imaging Coronary Anatomy and Reducing Myocardial Infarction Interval From Initiation of Prasugrel to Coronary Angiography in Patients With Non–ST-Segment Elevation Myocardial Infarction Multivessel PCI Guided by FFR or Angiography for Myocardial Infarction Inflammatory Bowel Disease and Acute Coronary Syndromes: From Pathogenesis to the Fine Line Between Bleeding and Ischemic Risk
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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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