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The management of secondary mitral regurgitation in patients with heart failure: a joint position statement from the Heart Failure Association (HFA), European Association of Cardiovascular Imaging (EACVI), European Heart Rhythm Association (EHRA), and European Association of Percutaneous Cardiovascular Interventions (EAPCI) of the ESC Rivaroxaban for Thromboprophylaxis in High-Risk Ambulatory Patients With Cancer Impact of Transcatheter Mitral Valve Repair on Preprocedural and Postprocedural Hospitalization Rates Prospective Evaluation of Transseptal TMVR for Failed Surgical Bioprostheses: MITRAL Trial Valve-in-Valve Arm 1-Year Outcomes Implications of the local hemodynamic forces on the formation and destabilization of neoatherosclerotic lesions Strain-Guided Management of Potentially Cardiotoxic Cancer Therapy Risk of Cardiovascular Diseases Among Older Breast Cancer Survivors in the United States: A Matched Cohort Study Ablation Versus Drug Therapy for Atrial Fibrillation in Heart Failure Results From the CABANA Trial Long-Term Outcomes of Patients With Mediastinal Radiation–Associated Coronary Artery Disease Undergoing Coronary Revascularization With Percutaneous Coronary Intervention and Coronary Artery Bypass Grafting Cardio-oncology: A Focus on Cardiotoxicity
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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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