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Outcomes of off- and on-hours admission in ST-segment elevation myocardial infarction patients undergoing primary percutaneous coronary intervention: A retrospective observational cohort study Complete Versus Culprit-Only Revascularization in STEMI: a Contemporary Review Acute Myocardial Infarction after Laboratory-Confirmed Influenza Infection Aspirin-Free Prasugrel Monotherapy Following Coronary Artery Stenting in Patients With Stable CAD: The ASET Pilot Study Inflammation: A New Target For CAD Treatment and Prevention Relation between door-to-balloon times and mortality after primary percutaneous coronary intervention over time: a retrospective study Recurrent Cardiovascular Events in Survivors of Myocardial Infarction with St-Segment Elevation (From the AMI-QUEBEC Study) Effect of Shorter Door-to-Balloon Times Over 20 Years on Outcomes of Patients With Anterior ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention Prognostic significance of QRS fragmentation and correlation with infarct size in patients with anterior ST-segment elevation myocardial infarction treated with percutaneous coronary intervention: Insights from the INFUSE-AMI trial Complete revascularisation versus treatment of the culprit lesion only in patients with ST-segment elevation myocardial infarction and multivessel disease (DANAMI-3—PRIMULTI): an open-label, randomised controlled 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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