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Best Practices for the Prevention of Radial Artery Occlusion After Transradial Diagnostic Angiography and Intervention An International Consensus Paper Myocardial Infarction Risk Stratification With a Single Measurement of High-Sensitivity Troponin I Open sesame technique in percutaneous coronary intervention for ST-elevation myocardial infarction Large-Bore Radial Access for Complex PCI: A Flash of COLOR With Some Shades of Grey Validation of High-Risk Features for Stent-Related Ischemic Events as Endorsed by the 2017 DAPT Guidelines Invasive Management of Acute Myocardial Infarction Complicated by Cardiogenic Shock: A Scientific Statement From the American Heart Association Coronary Angiography after Cardiac Arrest without ST-Segment Elevation Relation of prior statin and anti-hypertensive use to severity of disease among patients hospitalized with COVID-19: Findings from the American Heart Association’s COVID-19 Cardiovascular Disease Registry Refractory Angina: From Pathophysiology to New Therapeutic Nonpharmacological Technologies Prevalence, Presentation and Treatment of 'Balloon Undilatable' Chronic Total Occlusions: Insights from a Multicenter US Registry
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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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