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From ACE Inhibitors/ARBs to ARNIs in Coronary Artery Disease and Heart Failure (Part 2/5) Long-Term Durability of Transcatheter Heart Valves: Insights From Bench Testing to 25 Years Unexpectedly Low Natriuretic Peptide Levels in Patients With Heart Failure Pulmonary artery denervation to treat pulmonary arterial hypertension: the single-center, prospective, first-in-man PADN-1 study (first-in-man pulmonary artery denervation for treatment of pulmonary artery hypertension) Dual Antiplatelet Therapy Duration: Reconciling the Inconsistencies Guideline‐Directed Medical Therapy for Patients With Heart Failure With Midrange Ejection Fraction: A Patient‐Pooled Analysis From the KorHF and KorAHF Registries Heart Failure With Mid-Range (Borderline) Ejection Fraction: Clinical Implications and Future Directions Atrial Fibrillation and the Prognostic Performance of Biomarkers in Heart Failure The Role of Vascular Imaging in Guiding Routine Percutaneous Coronary Interventions: A Meta-Analysis of Bare Metal Stent and Drug-Eluting Stent Trials Dapagliflozin and Cardiovascular Outcomes in Type 2 Diabetes
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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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