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Systems of Care for ST-Segment–Elevation Myocardial Infarction: A Policy Statement From the American Heart Association Coronary flow velocity reserve predicts adverse prognosis in women with angina and noobstructive coronary artery disease: resultsfrom the iPOWER study Mode of Death in Heart Failure With Preserved Ejection Fraction When high‐volume PCI operators in high‐volume hospitals move to lower volume hospitals—Do they still maintain high volume and quality of outcomes? 稳定性冠心病诊断与治疗指南 Prevalence of Angina Among Primary Care Patients With Coronary Artery Disease Current Smoking and Prognosis After Acute ST-Segment Elevation Myocardial Infarction: New Pathophysiological Insights The spectrum of chronic coronary syndromes: genetics, imaging, and management after PCI and CABG Switching P2Y12-receptor inhibitors in patients with coronary artery disease Generalizing Intensive Blood Pressure Treatment to Adults With Diabetes Mellitus
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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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