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Burden of Cardiovascular Diseases in China, 1990-2016: Findings From the 2016 Global Burden of Disease Study Minimalist transcatheter aortic valve replacement: The new standard for surgeons and cardiologists using transfemoral access? Predictors and Clinical Outcomes of Next-Day Discharge After Minimalist Transfemoral Transcatheter Aortic Valve Replacement Longitudinal Assessment of Vascular Function With Sunitinib in Patients With Metastatic Renal Cell Carcinoma Diagnostic performance of noninvasive myocardial perfusion imaging using single-photon emission computed tomography, cardiac magnetic resonance, and positron emission tomography imaging for the detection of obstructive coronary artery disease: a meta-analysis Coronary calcification in the diagnosis of coronary artery disease Impaired Retinal Microvascular Function Predicts Long-Term Adverse Events in Patients with Cardiovascular Disease From Detecting the Vulnerable Plaque to Managing the Vulnerable Patient CT Angiographic and Plaque Predictors of Functionally Significant Coronary Disease and Outcome Using Machine Learning Increased Risk of Valvular Heart Disease in Systemic Sclerosis: An Underrecognized Cardiac Complication

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.