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Impact of intravascular ultrasound guidance in routine percutaneous coronary intervention for conventional lesions: data from the EXCELLENT trial Ambulatory Electrocardiogram Monitoring in Patients Undergoing Transcatheter Aortic Valve Replacement: JACC State-of-the-Art Review Impact of coronary anatomy and stenting technique on long-term outcome after drug-eluting stent implantation for unprotected left main coronary artery disease In vitro flow and optical coherence tomography comparison of two bailout techniques after failed provisional stenting for bifurcation percutaneous coronary interventions Association of Sustained Blood Pressure Control with Multimorbidity Progression Among Older Adults Differences between the left main and other bifurcations Leaflet immobility and thrombosis in transcatheter aortic valve replacement Pulmonary Artery Denervation Attenuates Pulmonary Arterial Remodeling in Dogs With Pulmonary Arterial Hypertension Induced by Dehydrogenized Monocrotaline Clinical and angiographic outcomes of patients treated with everolimus-eluting stents or first-generation Paclitaxel-eluting stents for unprotected left main disease Rationale and design of the comparison between a P2Y12 inhibitor monotherapy versus dual antiplatelet therapy in patients undergoing implantation of coronary drug-eluting stents (SMART-CHOICE): A prospective multicenter randomized trial
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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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