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An EAPCI Expert Consensus Document on Ischaemia with Non-Obstructive Coronary Arteries in Collaboration with European Society of Cardiology Working Group on Coronary Pathophysiology & Microcirculation Endorsed by Coronary Vasomotor Disorders International Study Group Association of Silent Myocardial Infarction and Sudden Cardiac Death Major trials in coronary intervention from 2018 Right ventricular stroke work correlates with outcomes in pediatric pulmonary arterial hypertension Prognostic Value of SYNTAX Score in Patients With Infarct-Related Cardiogenic Shock: Insights From the CULPRIT-SHOCK Trial Chronic Total Occlusion Percutaneous Coronary Intervention: Evidence and Controversies Subcutaneous Selatogrel Inhibits Platelet Aggregation in Patients With Acute Myocardial Infarction Impact of Chronic Total Coronary Occlusion Location on Long-term Survival After Percutaneous Coronary Intervention Association of Plaque Location and Vessel Geometry Determined by Coronary Computed Tomographic Angiography With Future Acute Coronary Syndrome–Causing Culprit Lesions Early versus delayed invasive intervention in acute coronary syndromes
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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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