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Correction of a pathogenic gene mutation in human embryos Door-to-balloon time and mortality among patients undergoing primary PCI Early Versus Standard Discharge After Transcatheter Aortic Valve Replacement: A Systematic Review and Meta-Analysis Clinical value of post-percutaneous coronary intervention fractional flow reserve value: A systematic review and meta-analysis Balloon-to-door time: emerging evidence for shortening hospital stay after primary PCI for STEMI Australian Trends in Procedural Characteristics and Outcomes in Patients Undergoing Percutaneous Coronary Intervention for ST-Elevation Myocardial Infarction Trends in early aspirin use among patients with acute myocardial infarction in China, 2001-2011: the China PEACE-Retrospective AMI study Incidence, Treatment, and Outcomes of Coronary Perforation During Chronic Total Occlusion Percutaneous Coronary Intervention Diagnostic performance of noninvasive fractional flow reserve derived from coronary computed tomography angiography in suspected coronary artery disease: the NXT trial (Analysis of Coronary Blood Flow Using CT Angiography: Next Steps) Temporal trends in percutaneous coronary interventions thru the drug eluting stent era: Insights from 18,641 procedures performed over 12-year period
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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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