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Aliskiren, Enalapril, or Aliskiren and Enalapril in Heart Failure Minimizing Permanent Pacemaker Following Repositionable Self-Expanding Transcatheter Aortic Valve Replacement Comparison of safety and periprocedural complications of transfemoral aortic valve replacement under local anaesthesia: minimalist versus complete Heart Team Dapagliflozin in Patients with Heart Failure and Reduced Ejection Fraction Heart Failure With Improved Ejection Fraction-Is it Possible to Escape One’s Past? Is Cardiac Diastolic Dysfunction a Part of Post-Menopausal Syndrome? Association of Cardiovascular Disease With Respiratory Disease From Focal Lipid Storage to Systemic Inflammation 2019 ACC/AHA/ASE Advanced Training Statement on Echocardiography (Revision of the 2003 ACC/AHA Clinical Competence Statement on Echocardiography): A Report of the ACC Competency Management Committee Transcatheter aortic-valve replacement with a self-expanding prosthesis

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.