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Antiplatelet therapy in patients with myocardial infarction without obstructive coronary artery disease 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The Task Force for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC) OPTIMAL USE OF LIPID-LOWERING THERAPY AFTER ACUTE CORONARY SYNDROMES: A Position Paper endorsed by the International Lipid Expert Panel (ILEP) Optimal Timing of Intervention in NSTE-ACS Without Pre-Treatment The EARLY Randomized Trial The Prognostic Significance of Periprocedural Infarction in the Era of Potent Antithrombotic Therapy: The PRAGUE-18 Substudy Systematic Review for the 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines From Early Pharmacology to Recent Pharmacology Interventions in Acute Coronary Syndromes European Bifurcation Club White Paper on Stenting Techniques for Patients With Bifurcated Coronary Artery Lesions Percutaneous Coronary Intervention for Chronic Total Occlusion—The Michigan Experience: Insights From the BMC2 Registry Discharge Against Medical Advice After Percutaneous Coronary Intervention in the United States
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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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