ArticleNature communications2017
MyD88 promotes myoblast fusion in a cell-autonomous manner.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 65 citations in OpenAlex.
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- Synaptic-like coupling of macrophages to myofibers regulates muscle repair.Current biology : CB · 2025Article
- The canonical ER stress IRE1α/XBP1 pathway mediates skeletal muscle wasting during pancreatic cancer cachexia.EMBO molecular medicine · 2025Article
- Signaling networks governing skeletal muscle growth, atrophy, and cachexiaSkeletal muscle · 2025Review
- Hyperactivation of Transforming Growth Factor-β-Activated Kinase 1 Causes Skeletal Muscle Pathology Reminiscent of Inflammatory Myopathies.The American journal of pathology · 2025Article
- Fiber-type vulnerability and proteostasis reprogramming in skeletal muscle during pancreatic cancer cachexia.bioRxiv : the preprint server for biology · 2025Article
- The human genetic variant rs6190 unveils Foxc1 and Arid5a as novel prometabolic targets of the glucocorticoid receptor in muscle.Science advances · 2025Article
- Integrated transcriptomics and metabolomics reveal the molecular characteristics and metabolic regulatory mechanisms among different muscles in Minxian black fur sheep.BMC genomics · 2025Article
- Fibroblast growth factor-inducible 14 regulates satellite cell self-renewal and expansion during skeletal muscle repair.JCI insight · 2025Article
- Fibroblast growth factor-inducible 14 regulates satellite cell self-renewal and expansion during skeletal muscle repair.bioRxiv : the preprint server for biology · 2025Article
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- Ammonia transporter RhBG initiates downstream signaling and functional responses by activating NFκB.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Molecular Mechanisms of Cachexia: A Review.Cells · 2024Review
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- Fn14 promotes myoblast fusion during regenerative myogenesis.Life science alliance · 2023Article
- The transcriptional regulator KLF15 is necessary for myoblast differentiation and muscle regeneration by activating FKBP5.The Journal of biological chemistry · 2023Article
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- Enveloped viruses pseudotyped with mammalian myogenic cell fusogens target skeletal muscle for gene delivery.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Myoblast fusion is an indispensable step for skeletal muscle development, postnatal growth, and regeneration. Myeloid differentiation primary response gene 88 (MyD88) is an adaptor protein that mediates Toll-like receptors and interleukin-1 receptor signaling. Here we report a cell-autonomous role of MyD88 in the regulation of myoblast fusion. MyD88 protein levels are increased during in vitro myogenesis and in conditions that promote skeletal muscle growth in vivo. Deletion of MyD88 impairs fusion of myoblasts without affecting their survival, proliferation, or differentiation. MyD88 regulates non-canonical NF-κB and canonical Wnt signaling during myogenesis and promotes skeletal muscle growth and overload-induced myofiber hypertrophy in mice. Ablation of MyD88 reduces myofiber size during muscle regeneration, whereas its overexpression promotes fusion of exogenous myoblasts to injured myofibers. Our study shows that MyD88 modulates myoblast fusion and suggests that augmenting its levels may be a therapeutic approach to improve skeletal muscle formation in degenerative muscle disorders.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.