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Mortality and morbidity in acutely ill adults treated with liberal versus conservative oxygen therapy (IOTA): a systematic review and meta-analysis Door to Balloon Time: Is There a Point That Is Too Short? Remote ischaemic conditioning and healthcare system delay in patients with ST-segment elevation myocardial infarction Patterns and associations between DAPT cessation and 2-year clinical outcomes in left main/proximal LAD versus other PCI: Results from the Patterns of Non-Adherence to Dual Antiplatelet Therapy in Stented Patients (PARIS) registry Percutaneous coronary intervention reduces mortality in myocardial infarction patients with comorbidities: Implications for elderly patients with diabetes or kidney disease Targeting the Immune System in Atherosclerosis: JACC State-of-the-Art Review Fine particulate air pollution and hospital admissions and readmissions for acute myocardial infarction in 26 Chinese cities Prevention, Diagnosis, and Management of Radiation-Associated Cardiac Disease: JACC Scientific Expert Panel Obesity, Diabetes, and Acute Coronary Syndrome: Differences Between Asians and Whites Coronary Catheterization and Percutaneous Coronary Intervention in China: 10-Year Results From the China PEACE-Retrospective CathPCI Study
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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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