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Dapagliflozin Effects on Biomarkers, Symptoms, and Functional Status in Patients With Heart Failure With Reduced Ejection Fraction: The DEFINE-HF Trial Everolimus-Eluting Bioresorbable Scaffolds Versus Everolimus-Eluting Metallic Stents Transcatheter or Surgical Aortic-Valve Replacement in Intermediate-Risk Patients Correlation between frequency-domain optical coherence tomography and fractional flow reserve in angiographically-intermediate coronary lesions Evidence-based detection of pulmonary arterial hypertension in systemic sclerosis: the DETECT study How Low to Go With Glucose, Cholesterol, and Blood Pressure in Primary Prevention of CVD FFR-guided multivessel stenting reduces urgent revascularization compared with infarct-related artery only stenting in ST-elevation myocardial infarction: A meta-analysis of randomized controlled trials Surgical or Transcatheter Aortic-Valve Replacement in Intermediate-Risk Patients Lack of Association Between Heart Failure and Incident Cancer Frequency of nonsystem delays in ST-elevation myocardial infarction patients undergoing primary percutaneous coronary intervention and implications for door-to-balloon time reporting (from the American Heart Association Mission: Lifeline program)
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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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