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cardiomyocytes

Inhibition of MicroRNA-30a Alleviates Vascular Remodeling in Pulmonary Arterial Hypertension

[Molecular Therapy-Nucleic Acids] Researchers investigated the role of miR-30a in the pulmonary artery smooth muscle cells remodeling of pulmonary arterial hypertension.

Insulin-Like Growth Factor Binding Protein-1 Regulates HIF-1α-1α Degradation to Inhibit Apoptosis in Hypoxic Cardiomyocytes

[Cell Death Discovery] The authors demonstrated that hypoxia up-regulated IGFBP-1 and HIF-1α protein expression in cardiomyocytes. Subsequent assays showed that IGFBP-1 suppression decreased HIF-1α expression and inhibited hypoxia-induced apoptosis in cardiomyocytes, which was reversed by HIF-1α overexpression, indicating that HIF-1α was essential to IGFBP-1 function in cellular apoptosis.

Histone Deacetylase HDAC4 Participates in the Pathological Process of Myocardial Ischemia-Reperfusion Injury via MEKK1/JNK Pathway by Binding to miR-206

[Cell Death Discovery] Investigators defined the underlying role of histone deacetylase 4 (HDAC4) and miR-206 in the pathological process of myocardial ischemia-reperfusion injury (MIRI). Up-regulation of HDAC4 and down-regulation of miR-206 occurred in rat myocardial tissues and cardiomyocytes in MIRI.

RARG Variant Predictive of Doxorubicin-Induced Cardiotoxicity Identifies a Cardioprotective Therapy

[Current Biology] Researchers showed that human induced pluripotent stem cell-derived cardiomyocytes from patients with rs2229774 and who suffered doxorubicin-induced cardiotoxicity were more sensitive to doxorubicin.

Asiatic Acid Alleviates Ischemic Myocardial Injury in Mice by Modulating Mitophagy- and Glycophagy-Based Energy Metabolism

[Acta Pharmacologica Sinica] Scientists investigated whether asiatic acid exerted cardioprotective effects against myocardial infarction by activating glycophagy and mitophagy to improve the energy balance. In vitro cardioprotective effects were examined in neonatal mouse cardiomyocytes subjected to oxygen-glucose deprivation for 12 hours.

Interleukin-11 Signaling Promotes Cellular Reprogramming and Limits Fibrotic Scarring during Tissue Regeneration

[Science Advances] Investigators indicated that interleukin-11 signaling in endothelial cells antagonized profibrotic transforming growth factor–β signaling and endothelial-to-mesenchymal transition, limiting scarring and promoting cardiomyocyte repopulation, after injury.

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