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Long-term Survival following Multivessel Revascularization in Patients with Diabetes (FREEDOM Follow-On Study) Radial Versus Femoral Access for Coronary Interventions Across the Entire Spectrum of Patients With Coronary Artery Disease: A Meta-Analysis of Randomized Trials Classic crush and DK crush stenting techniques The prognostic role of mid-range ejection fraction in ST-segment elevation myocardial infarction Coronary Artery Plaque Characteristics Associated With Adverse Outcomes in the SCOT-HEART Study The HACD4 haplotype as a risk factor for atherosclerosis in males Changes in One-Year Mortality in Elderly Patients Admitted with Acute Myocardial Infarction in Relation with Early Management LOX-1 in Atherosclerosis and Myocardial Ischemia: Biology, Genetics, and Modulation The association between body mass index and obesity with survival in pulmonary arterial hypertension A sirolimus-eluting bioabsorbable polymer-coated stent (MiStent) versus an everolimus-eluting durable polymer stent (Xience) after percutaneous coronary intervention (DESSOLVE III): a randomised, single-blind, multicentre, non-inferiority, phase 3 trial
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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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