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Nonculprit Lesion Myocardial Infarction Following Percutaneous Coronary Intervention in Patients With Acute Coronary Syndrome Prognostic value of fibrinogen in patients with coronary artery disease and prediabetes or diabetes following percutaneous coronary intervention: 5-year findings from a large cohort study Implications of Alternative Definitions of Peri-Procedural Myocardial Infarction After Coronary Revascularization Risk Factors Associated With Major Cardiovascular Events 1 Year After Acute Myocardial Infarction Colchicine Inhibits Neutrophil Extracellular Trap Formation in Patients With Acute Coronary Syndrome After Percutaneous Coronary Intervention 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines Mild Hypothermia in Cardiogenic Shock Complicating Myocardial Infarction - The Randomized SHOCK-COOL Trial Early Natural History of Spontaneous Coronary Artery Dissection Impact of Percutaneous Coronary Intervention for Chronic Total Occlusion in Non-Infarct-Related Arteries in Patients With Acute Myocardial Infarction (from the COREA-AMI Registry) Characterization of lesions undergoing ischemia-driven revascularization after complete revascularization versus culprit lesion only in patients with STEMI and multivessel disease - A DANAMI-3-PRIMULTI substudy
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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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