ArticleCell death & disease2015
Myocyte-derived Tnfsf14 is a survival factor necessary for myoblast differentiation and skeletal muscle regeneration.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Environmental PFOA Exposure Alters Early Developmental Programming during the Maternal-Zygotic Transition.bioRxiv : the preprint server for biology · 2026Article
- Role of LIGHT in the Inflammatory Mechanisms of Psoriasis via Upregulation of Proliferation and Cytokine Production of Keratinocytes.Immunity, inflammation and disease · 2026Article
- The maternal-to-zygotic transition is a critical window for PFOA-induced disruption of developmental programming.Frontiers in cell and developmental biology · 2026Article
- A non-invasive mouse model that recapitulates disuse-induced muscle atrophy in immobilized patients.Scientific reports · 2023Article
- Nonsense-mediated mRNA decay promote C2C12 cell proliferation by targeting PIK3R5.Journal of muscle research and cell motility · 2023Article
- TNFSF14-Derived Molecules as a Novel Treatment for Obesity and Type 2 Diabetes.International journal of molecular sciences · 2021Article
- Article
- The Role of TNF Family Molecules Light in Cellular Interaction Between Airway Smooth Muscle Cells and T Cells During Chronic Allergic Inflammation.Inflammation · 2018Article
- Myogenic regulatory factors: The orchestrators of myogenesis after 30 years of discovery.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- NDRG4 promotes myogenesis via Akt/CREB activation.Oncotarget · 2017Article
- Cxcl14 depletion accelerates skeletal myogenesis by promoting cell cycle withdrawal.NPJ Regenerative medicine · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Adult skeletal muscle tissue has a uniquely robust capacity for regeneration, which gradually declines with aging or is compromised in muscle diseases. The cellular mechanisms regulating adult myogenesis remain incompletely understood. Here we identify the cytokine tumor necrosis factor superfamily member 14 (Tnfsf14) as a positive regulator of myoblast differentiation in culture and muscle regeneration in vivo. We find that Tnfsf14, as well as its cognate receptors herpes virus entry mediator (HVEM) and lymphotoxin β receptor (LTβR), are expressed in both differentiating myocytes and regenerating myofibers. Depletion of Tnfsf14 or either receptor inhibits myoblast differentiation and promotes apoptosis. Our results also suggest that Tnfsf14 regulates myogenesis by supporting cell survival and maintaining a sufficient pool of cells for fusion. In addition, we show that Akt mediates the survival and myogenic function of Tnfsf14. Importantly, local knockdown of Tnfsf14 is found to impair injury-induced muscle regeneration in a mouse model, affirming an important physiological role for Tnfsf14 in myogenesis in vivo. Furthermore, we demonstrate that localized overexpression of Tnfsf14 potently enhances muscle regeneration, and that this regenerative capacity of Tnfsf14 is dependent on Akt signaling. Taken together, our findings reveal a novel regulator of skeletal myogenesis and implicate Tnfsf14 in future therapeutic development.
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