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Clinical applications of machine learning in the diagnosis, classification, and prediction of heart failure Rationale and design of the GUIDE-IT study: Guiding Evidence Based Therapy Using Biomarker Intensified Treatment in Heart Failure Comprehensive intravascular ultrasound assessment of stent area and its impact on restenosis and adverse cardiac events in 403 patients with unprotected left main disease From Subclinical Atherosclerosis to Plaque Progression and Acute Coronary Events Primary Prevention of Sudden Cardiac Death The year in cardiology: heart failure: The year in cardiology 2019 Prevalence and clinical implications of valvular calcification on coronary computed tomography angiography Association of Abnormal Left Ventricular Functional Reserve With Outcome in Heart Failure With Preserved Ejection Fraction Percutaneous Atriotomy for Levoatrial–to–Coronary Sinus Shunting in Symptomatic Heart Failure: First-in-Human Experience Poor Long-Term Survival in Patients With Moderate Aortic Stenosis
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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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