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The right ventricle in pulmonary hypertension Increased pulmonary serotonin transporter in patients with chronic obstructive pulmonary disease who developed pulmonary hypertension Fractional flow reserve-guided PCI versus medical therapy in stable coronary disease Prognostic Implication of Thermodilution Coronary Flow Reserve in Patients Undergoing Fractional Flow Reserve Measurement Clinical Outcomes and Cost-Effectiveness of Fractional Flow Reserve-Guided Percutaneous Coronary Intervention in Patients With Stable Coronary Artery Disease: Three-Year Follow-Up of the FAME 2 Trial (Fractional Flow Reserve Versus Angiography for Multivessel Evaluation) Diagnosis of ischemia-causing coronary stenoses by noninvasive fractional flow reserve computed from coronary computed tomographic angiograms. Results from the prospective multicenter DISCOVER-FLOW Patient and Hospital Characteristics of Mitral Valve Surgery in the United States Relationship between fractional flow reserve value and the amount of subtended myocardium Independent Association of Lipoprotein(a) and Coronary Artery Calcification With Atherosclerotic Cardiovascular Risk Fractional Flow Reserve-Guided Multivessel Angioplasty in Myocardial Infarction
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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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