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The prevalence and importance of frailty in heart failure with reduced ejection fraction - an analysis of PARADIGM-HF and ATMOSPHERE Contemporary real-world outcomes of surgical aortic valve replacement in 141,905 low-risk, intermediate-risk, and high-risk patients rhACE2 Therapy Modifies Bleomycin-Induced Pulmonary Hypertension via Rescue of Vascular Remodeling A trial to evaluate the effect of the sodium-glucose co-transporter 2 inhibitor dapagliflozin on morbidity and mortality in patients with heart failure and reduced left ventricular ejection fraction (DAPA-HF) The Objective Physical Activity and Cardiovascular Disease Health in Older Women (OPACH) Study The Management of Atrial Fibrillation in Heart Failure: An Expert Panel Consensus Metabolic Interactions and Differences between Coronary Heart Disease and Diabetes Mellitus: A Pilot Study on Biomarker Determination and Pathogenesis Cardiovascular Considerations in Caring for Pregnant Patients: A Scientific Statement From the American Heart Association Optical coherence tomography and intravascular ultrasound assessment of the anatomic size and wall thickness of a muscle bridge segment Circadian-Regulated Cell Death in Cardiovascular Diseases
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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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