ArticleActa biochimica et biophysica Sinica2024
Skeletal muscle-derived musclin attenuates glycolysis, oxidative stress, and pulmonary hypertension through the NPR3/AKT/mTORC1 pathway.
Article in Acta biochimica et biophysica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- LMS-based continuous reference values for the myokine musclin in serum in children and adults.Frontiers in endocrinology · 2026Article
- Inhibition of vascular intimal hyperplasia by the myokine Musclin: the role of NPR3/raptor/mTORC1-mediated glycolysis and phenotypic switching of VSMCs.Acta biochimica et biophysica Sinica · 2025Article
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7 authors.
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Abstract
Exercise ameliorates pulmonary hypertension (PH) progression. However, the underlying mechanisms are largely unclear. Musclin is an exercise-responsive myokine that exerts protective effects on cardiovascular diseases. The current study aims to explore the role of musclin in the development of PH. A monocrotaline (MCT)-induced mouse PH model is established. Adeno-associated virus serotype 6 (AAV6)-mediated gene transfer is used to induce musclin overexpression in skeletal muscle. Ultrasound and morphological analyses are utilized to assess the severity of PH. Cell viability assay, Ki-67 immunofluorescence staining, wound healing assay, and transwell assay are used to evaluate the proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs). We find that the musclin levels in both plasma and skeletal muscle are decreased in MCT-treated mice. The external expression of musclin in skeletal muscle ameliorates pulmonary arterial remodeling and right ventricular dysfunction.
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