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muscle cells

Transcriptomic Characterization of the Molecular Mechanisms Induced by RGMa during Skeletal Muscle Nuclei Accretion and Hypertrophy

[BMC Genomics] RGMa expression patterns and signaling pathways via Neogenin and/or as BMP coreceptors indicated that this axon guidance molecule could also be working in other processes and diseases, including during myogenesis.

Intercellular Transfer of miR-200c-3p Impairs the Angiogenic Capacity of Cardiac Endothelial Cells

[Molecular Therapy] Researchers reported that cardiac stress-induced differential microRNA content, with miR-200c-3p being one of the most enriched, in cardiomyocyte-derived extracellular vesicles mediates functional crosstalk with endothelial cells.

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.

The Circular RNA circNlgn Mediates Doxorubicin-Induced Cardiac Remodeling and Fibrosis

[Molecular Therapy-Nucleic Acids] Scientists developed a transgenic mouse line overexpressing the circular RNA circNlgn and showed that circNlgn was a mediator of Doxorubicin-induced cardio-fibrosis.

Doxorubicin Induces Cardiotoxicity in a Pluripotent Stem Cell Model of Aggressive B Cell Lymphoma Cancer Patients

[Basic Research in Cardiology] Researchers established an in vitro iPSC model of anthracycline-induced cardiotoxicity (ACT) from patients with an aggressive form of B-cell lymphoma and examined whether doxorubicin-treated ACT-iPSC cardiomyocytes could recapitulate the clinical features exhibited by patients.

Platelet-Derived TGF (Transforming Growth Factor)-β1 Enhances the Aerobic Glycolysis of Pulmonary Arterial Smooth Muscle Cells by PKM2 Upregulation

[Hypertension] Researchers investigated pulmonary arterial smooth muscle cell aerobic glycolysis after being treated with platelet supernatant. TGF-βRI, PKM2, and other antagonists were applied to identify the underlying mechanism

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