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Prevalence of potential drug-drug interactions in cancer patients treated with oral anticancer drugs Coronary Calcification and Long-Term Outcomes According to Drug-Eluting Stent Generation The Regulation of Pulmonary Vascular Tone by Neuropeptides and the Implications for Pulmonary Hypertension Association Between Malignant Mitral Valve Prolapse and Sudden Cardiac Death: A Review Thrombotic Risk and Antithrombotic Strategies After Transcatheter Mitral Valve Replacement Benefits with drug-coated balloon as compared to a conventional revascularization strategy for the treatment of coronary and non-coronary arterial disease: a comprehensive meta-analysis of 45 randomized trials Five-Year Clinical Outcomes After Drug-Eluting Stent Implantation Following Rotational Atherectomy for Heavily Calcified Lesions Orbital atherectomy for the treatment of small (2.5mm) severely calcified coronary lesions: ORBIT II sub-analysis Optical Coherence Tomography to Assess Proximal Side Optimization Technique in Crush Stenting Initial experience with percutaneous mitral valve repair in patients with cardiac amyloidosis
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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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