Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (737 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Developmental events leading to the formation of adult muscular system, which includes differentiation of the various types of muscle cell precursors, migration of myoblasts, activation of myogenesis and development of muscle anchorage.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Development, Muscle; Muscular Development; Development, Muscular; Myogenesis; Myofibrillogenesis.
Where it fits in the MeSH classification
- Broader topics
- Musculoskeletal Development
- Narrower topics
- Skeletal Muscle Enlargement
Research landscape
PubMed indexes 11,528 records tagged with the MeSH heading “Muscle Development” (counts retrieved 2026-10-31). 2,355 of them (20.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 3,889 records.
Reviews account for 1,202 records (10.4%) and meta-analyses for 13. Randomized controlled trials number 72 (0.6%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 3,889 |
| 2000-2009 | 1,660 |
| 2010-2019 | 3,624 |
| 2020 onward | 2,355 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,202 | 10.4% |
| Meta-analyses | 13 | 0.1% |
| Randomized controlled trials | 72 | 0.6% |
Method: PubMed query "Muscle Development"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Origins, potency, and heterogeneity of skeletal muscle fibro-adipogenic progenitors-time for new definitions | 2021 | Review article Design not recorded in structured metadata | 132 | cc by PMID 34210364 · DOI · PMC8247239 |
| Resolvin-D2 targets myogenic cells and improves muscle regeneration in Duchenne muscular dystrophy | 2021 | Research article Design not recorded in structured metadata | 69 | cc by PMID 34716330 · DOI · PMC8556273 |
| CircRNA-Protein Interactions in Muscle Development and Diseases | 2021 | Review article Design not recorded in structured metadata | 65 | cc by PMID 33806945 · DOI · PMC8005172 |
| Effects of Skeletal Muscle Hypertrophy on Fat Mass and Glucose Homeostasis in Humans and Animals: A Narrative Review with Systematic Literature Search | 2025 | Systematic review Design not recorded in structured metadata | 18 | cc by PMID 40576707 · DOI · PMC12460530 |
Origins, potency, and heterogeneity of skeletal muscle fibro-adipogenic progenitors-time for new definitions [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Striated muscle is a highly plastic and regenerative organ that regulates body movement, temperature, and metabolism-all the functions needed for an individual's health and well-being.
- Closing excerpt
- Thus, this compelling review provides new cellular and molecular insights in comprehending the origins, definitions, markers, fate, and plasticity of murine and human fibro-adipogenic progenitors in muscle development, homeostasis, regeneration, and repair.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (188 words)
Striated muscle is a highly plastic and regenerative organ that regulates body movement, temperature, and metabolism-all the functions needed for an individual's health and well-being. The muscle connective tissue's main components are the extracellular matrix and its resident stromal cells, which continuously reshape it in embryonic development, homeostasis, and regeneration. Fibro-adipogenic progenitors are enigmatic and transformative muscle-resident interstitial cells with mesenchymal stem/stromal cell properties. They act as cellular sentinels and physiological hubs for adult muscle homeostasis and regeneration by shaping the microenvironment by secreting a complex cocktail of extracellular matrix components, diffusible cytokines, ligands, and immune-modulatory factors. Fibro-adipogenic progenitors are the lineage precursors of specialized cells, including activated fibroblasts, adipocytes, and osteogenic cells after injury. Here, we discuss current research gaps, potential druggable developments, and outstanding questions about fibro-adipogenic progenitor origins, potency, and heterogeneity. Finally, we took advantage of recent advances in single-cell technologies combined with lineage tracing to unify the diversity of stromal fibro-adipogenic progenitors. Thus, this compelling review provides new cellular and molecular insights in comprehending the origins, definitions, markers, fate, and plasticity of murine and human fibro-adipogenic progenitors in muscle development, homeostasis, regeneration, and repair.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34210364 · DOI · PMC8247239
Resolvin-D2 targets myogenic cells and improves muscle regeneration in Duchenne muscular dystrophy [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Lack of dystrophin causes muscle degeneration, which is exacerbated by chronic inflammation and reduced regenerative capacity of muscle stem cells in Duchenne Muscular Dystrophy (DMD).
- Closing excerpt
- Overall, this preclinical study has identified a new therapeutic approach that is more potent than the gold-standard treatment for DMD.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (203 words)
Lack of dystrophin causes muscle degeneration, which is exacerbated by chronic inflammation and reduced regenerative capacity of muscle stem cells in Duchenne Muscular Dystrophy (DMD). To date, glucocorticoids remain the gold standard for the treatment of DMD. These drugs are able to slow down the progression of the disease and increase lifespan by dampening the chronic and excessive inflammatory process; however, they also have numerous harmful side effects that hamper their therapeutic potential. Here, we investigated Resolvin-D2 as a new therapeutic alternative having the potential to target multiple key features contributing to the disease progression. Our in vitro findings showed that Resolvin-D2 promotes the switch of macrophages toward their anti-inflammatory phenotype and increases their secretion of pro-myogenic factors. Moreover, Resolvin-D2 directly targets myogenic cells and promotes their differentiation and the expansion of the pool of myogenic progenitor cells leading to increased myogenesis. These effects are ablated when the receptor Gpr18 is knocked-out, knocked-down, or blocked by the pharmacological antagonist O-1918. Using different mouse models of DMD, we showed that Resolvin-D2 targets both inflammation and myogenesis leading to enhanced muscle function compared to glucocorticoids. Overall, this preclinical study has identified a new therapeutic approach that is more potent than the gold-standard treatment for DMD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34716330 · DOI · PMC8556273
CircRNA-Protein Interactions in Muscle Development and Diseases [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Circular RNA (circRNA) is a kind of novel endogenous noncoding RNA formed through back-splicing of mRNA precursor.
- Closing excerpt
- Our review reveals the significance of circRNAs and their protein chaperones and provides a reference for further study in this field.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (124 words)
Circular RNA (circRNA) is a kind of novel endogenous noncoding RNA formed through back-splicing of mRNA precursor. The biogenesis, degradation, nucleus-cytoplasm transport, location, and even translation of circRNA are controlled by RNA-binding proteins (RBPs). Therefore, circRNAs and the chaperoned RBPs play critical roles in biological functions that significantly contribute to normal animal development and disease. In this review, we systematically characterize the possible molecular mechanism of circRNA-protein interactions, summarize the latest research on circRNA-protein interactions in muscle development and myocardial disease, and discuss the future application of circRNA in treating muscle diseases. Finally, we provide several valid prediction methods and experimental verification approaches. Our review reveals the significance of circRNAs and their protein chaperones and provides a reference for further study in this field.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33806945 · DOI · PMC8005172
Effects of Skeletal Muscle Hypertrophy on Fat Mass and Glucose Homeostasis in Humans and Animals: A Narrative Review with Systematic Literature Search [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Overweight, obesity, and type 2 diabetes mellitus are metabolic health problems and diseases that affect billions of people worldwide.
- Closing excerpt
- We also discuss the potential use of hypertrophy-focused resistance training and muscle hypertrophy-stimulating drugs as treatments for people with overweight, obesity, and type 2 diabetes.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (222 words)
Overweight, obesity, and type 2 diabetes mellitus are metabolic health problems and diseases that affect billions of people worldwide. Studies in animals and humans suggest that stimulating global muscle hypertrophy could be a treatment for these diseases, as some key studies suggest that stimulation of global muscle hypertrophy commonly reduces fat mass and improves glucose homeostasis. To analyse the effect of muscle hypertrophy on fat and glucose homeostasis in more detail, we systematically searched the literature and quantitatively analyzed 122 studies (humans: n = 99; animals: n = 23). This analysis reveals that a 1.9-3.3% increase in global muscle mass in humans is associated with 4.1 ± 5.8% lower fat mass, a mean relative reduction in HbA1c of 4.1 ± 4.6% from baseline, and a reduction of fasting glucose concentrations by 5.8 ± 7.3% in studies lasting 2 weeks to 3 years. In the animal studies analyzed, the researchers increased muscle mass by transgenesis, drugs, or resistance training by 17.7 ± 18.4%. This increase of muscle mass was associated with 23.7 ± 22.3% less fat mass. In the second part of this review, we discuss mechanisms by which muscle hypertrophy can affect fat mass and glucose homeostasis. We also discuss the potential use of hypertrophy-focused resistance training and muscle hypertrophy-stimulating drugs as treatments for people with overweight, obesity, and type 2 diabetes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40576707 · DOI · PMC12460530
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Satellite cells and the muscle stem cell niche [5]
- Research article Building muscle: molecular regulation of myogenesis [6]
- Research article Making muscle: skeletal myogenesis in vivo and in vitro [7]
- Research article The mechanisms of muscle hypertrophy and their application to resistance training [8]
- Research article Protein supplementation augments the adaptive response of skeletal muscle to resistance-type exercise training: a meta-analysis [9]
- Research article The myogenic regulatory factors, determinants of muscle development, cell identity and regeneration [10]
References
- Contreras O, Rossi FMV, Theret M. Origins, potency, and heterogeneity of skeletal muscle fibro-adipogenic progenitors-time for new definitions. . 2021. PMID 34210364 · DOI · PMC8247239
- Dort J, Orfi Z, Fabre P, Molina T, Conte TC, Greffard K, et al.. Resolvin-D2 targets myogenic cells and improves muscle regeneration in Duchenne muscular dystrophy. . 2021. PMID 34716330 · DOI · PMC8556273
- Zheng S, Zhang X, Odame E, Xu X, Chen Y, Ye J, et al.. CircRNA-Protein Interactions in Muscle Development and Diseases. . 2021. PMID 33806945 · DOI · PMC8005172
- Havers T, Held S, Schönfelder M, Geisler S, Wackerhage H. Effects of Skeletal Muscle Hypertrophy on Fat Mass and Glucose Homeostasis in Humans and Animals: A Narrative Review with Systematic Literature Search. . 2025. PMID 40576707 · DOI · PMC12460530
- Yin H, Price F, Rudnicki MA. Satellite cells and the muscle stem cell niche. Physiol Rev. 2013. PMID 23303905 · DOI · PMC4073943
- Bentzinger CF, Wang YX, Rudnicki MA. Building muscle: molecular regulation of myogenesis. Cold Spring Harb Perspect Biol. 2012. PMID 22300977 · DOI · PMC3281568
- Chal J, Pourquié O. Making muscle: skeletal myogenesis in vivo and in vitro. Development. 2017. PMID 28634270 · DOI
- Schoenfeld BJ. The mechanisms of muscle hypertrophy and their application to resistance training. J Strength Cond Res. 2010. PMID 20847704 · DOI
- Cermak NM, Res PT, de Groot LC, Saris WH, van Loon LJ. Protein supplementation augments the adaptive response of skeletal muscle to resistance-type exercise training: a meta-analysis. Am J Clin Nutr. 2012. PMID 23134885 · DOI
- Hernández-Hernández JM, García-González EG, Brun CE, Rudnicki MA. The myogenic regulatory factors, determinants of muscle development, cell identity and regeneration. Semin Cell Dev Biol. 2017. PMID 29127045 · DOI · PMC5723221
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.