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Individualized antiplatelet therapy after drug-eluting stent deployment: Implication of clinical trials of different durations of dual antiplatelet therapy Valve‐in‐Valve for Degenerated Transcatheter Aortic Valve Replacement Versus Valve‐in‐Valve for Degenerated Surgical Aortic Bioprostheses: A 3‐Center Comparison of Hemodynamic and 1‐Year Outcome The role of integrated backscatter intravascular ultrasound in characterizing bare metal and drug-eluting stent restenotic neointima as compared to optical coherence tomography 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure Intravascular ultrasound predictors of angiographic restenosis after sirolimus-eluting stent implantation Complex PCI procedures: challenges for the interventional cardiologist Prospective application of pre-defined intravascular ultrasound criteria for assessment of intermediate left main coronary artery lesions results from the multicenter LITRO study Intravascular Ultrasound Guidance vs. Angiographic Guidance in Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction - Long-Term Clinical Outcomes From the CREDO-Kyoto AMI Registry Differential Impact of Heart Failure With Reduced Ejection Fraction on Men and Women Value of Coronary Artery Calcium Scanning in Association With the Net Benefit of Aspirin in Primary Prevention of Atherosclerotic Cardiovascular Disease
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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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