CBS 2019
CBSMD教育中心
English

科学研究

科研文章

荐读文献

Left Atrial Appendage Closure versus Non-Warfarin Oral Anticoagulation in Atrial Fibrillation: 4-Year Outcomes of PRAGUE-17 Frailty and Clinical Outcomes of Direct Oral Anticoagulants Versus Warfarin in Older Adults With Atrial Fibrillation: A Cohort Study Patent Foramen Ovale Attributable Cryptogenic Embolism With Thrombophilia Has Higher Risk for Recurrence and Responds to Closure Alcohol consumption, cardiac biomarkers, and risk of atrial fibrillation and adverse outcomes Role of endothelial dysfunction in determining angina after percutaneous coronary intervention: Learning from pathophysiology to optimize treatment Stretch-induced sarcoplasmic reticulum calcium leak is causatively associated with atrial fibrillation in pressure-overloaded hearts Transcatheter Aortic Valve Implantation Represents an Anti-Inflammatory Therapy Via Reduction of Shear Stress-Induced, Piezo-1-Mediated Monocyte Activation Systematic Review and Network Meta‐Analysis Comparing Bifurcation Techniques for Percutaneous Coronary Intervention Residual Shunt After Patent Foramen Ovale Closure and Long-Term Stroke Recurrence: A Prospective Cohort Study Potential Candidates for Transcatheter Tricuspid Valve Intervention After Transcatheter Aortic Valve Replacement: Predictors and Prognosis

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.