Tag results:

myocardial infarction

A Small-Molecule Cocktail Promotes Mammalian Cardiomyocyte Proliferation and Heart Regeneration

[Cell Stem Cell] Investigators reported a chemical cocktail of five small molecules that promoted adult cardiomyocyte proliferation and heart regeneration.

LncRNA FAF Attenuates Hypoxia/Ischaemia-Induced Pyroptosis via the miR-185-5p/PAK2 Axis in Cardiomyocytes

[Journal of Cellular and Molecular Medicine] Investigators explored the antipyroptotic effects of long noncoding RNA (lncRNA) FGF9-associated factor (FAF) in acute myocardial infarction.

Monocyte Subpopulation Profiling Indicates CDK6-Derived Cell Differentiation and Identifies Subpopulation-Specific miRNA Expression Sets in Acute and Stable Coronary Artery Disease

[Scientific Reports] Investigators characterized monocyte subsets in controls and disease phenotypes of coronary artery disease and mmyocardial infarction patients using flow cytometry and miRNA and mRNA expression profiling using RNA sequencing.

EZH2 Mitigates the Cardioprotective Effects of Mesenchymal Stem Cell-Secreted Exosomes against Infarction via HMGA2-Mediated PI3K/AKT Signaling

[BMC Cardiovascular Disorders] Investigators probed the therapeutic effects of MSC-derived exosomes on myocardial fibrosis after myocardial infarction and possible mechanisms.

Sox9 Promotes Cardiomyocyte Apoptosis after Acute Myocardial Infarction by Promoting miR-223-3p and Inhibiting MEF2C

[Molecular Biotechnology] Researchers probe the role of Sox9 in cardiomyocyte apoptosis after acute myocardial infarction (AMI). AMI cell model was established in AC16 cells by hypoxia treatment.

Human Umbilical Cord Mesenchymal Stem Cell-Derived Extracellular Vesicles Loaded with miR-223 Ameliorate Myocardial Infarction through P53/S100A9 Axis

[Genomics] Scientists explored the mechanism of human umbilical cord mesenchymal stem cells-derived extracellular vesicles loaded with miR-223 on myocardial infarction. Inflammation, cell biological functions, and fibrosis in vitro were measured.