# Mouse Models of Muscle Fibrosis: Mechanisms, Methods, and Applications

**Authors:** Sarah E. DiIorio, Mia J. Fowler, Bill Young, Michelle F. Griffin, Michael T. Longaker

PMC · DOI: 10.3390/biomedicines14020328 · Biomedicines · 2026-01-31

## TL;DR

This review discusses mouse models of muscle fibrosis to understand injury, repair, and ways to reduce fibrosis and promote regeneration.

## Contribution

The paper provides a comprehensive overview of mouse models for studying muscle fibrosis and highlights areas for future research.

## Key findings

- Mouse models like volumetric muscle loss and myotoxin injection are widely used to study muscle fibrosis.
- Histological, cellular, and molecular outcome measures are commonly used in these models.
- Expanding studies on muscle fibrosis could reveal new mechanisms to reduce fibrosis and enhance regeneration.

## Abstract

Skeletal muscle injuries are common and some are able to regenerate due to satellite cells, the muscle stem cell population. However, in cases of severe muscle injury, complete tears, or muscle loss via trauma, muscles can undergo fibrosis and long-term compromise of their structure and function. The development of animal models has been key to understanding the pathways involved in muscle injury, fibrosis, and repair. In this review, we discuss the animal models currently used, with a focus on those most applicable to studying muscle fibrosis after traumatic injury. We summarize the approach, findings, and limitations of the most widely used models, including volumetric muscle loss, laceration, and myotoxin injection studies, and provide a brief description of ischemia/reperfusion, crush injury, freeze injury, and dystrophy models. We summarize the histological, cellular, molecular, and functional outcome measures commonly used in the field and outline areas for translation and future work. An expansion of current studies to specifically focus on muscle fibrosis will surely elucidate novel mechanisms for reducing debilitating fibrosis and promoting regeneration.

## Linked entities

- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** FAP (fibroblast activation protein alpha) [NCBI Gene 2191] {aka DPPIV, FAPA, FAPalpha, SIMP}, CREG1 (cellular repressor of E1A stimulated genes 1) [NCBI Gene 8804] {aka CREG}, Pdgfrb (platelet derived growth factor receptor, beta polypeptide) [NCBI Gene 18596] {aka CD140b, PDGFR-1, Pdgfr}, Pla2g1b (phospholipase A2, group IB, pancreas) [NCBI Gene 18778] {aka Pla2a, sPLA2IB}, MEGF10 (multiple EGF like domains 10) [NCBI Gene 84466] {aka CMYO10A, CMYO10B, CMYP10A, CMYP10B, EMARDD, SR-F3}, Igf1 (insulin-like growth factor 1) [NCBI Gene 16000] {aka C730016P09Rik, Igf-1, Igf-I}, Tgfb1 (transforming growth factor, beta 1) [NCBI Gene 21803] {aka TGF-beta1, TGFbeta1, Tgfb, Tgfb-1}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}, FN1 (fibronectin 1) [NCBI Gene 2335] {aka CIG, ED-B, FINC, FN, FNZ, GFND}, DMD (dystrophin) [NCBI Gene 1756] {aka BMD, CMD3B, DXS142, DXS164, DXS206, DXS230}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}
- **Diseases:** traumatic accidents (MESH:D000081084), muscle scarring (MESH:D002921), Volumetric Muscle Loss (MESH:D009135), muscle degeneration (MESH:D009410), contusion (MESH:D003288), degenerative musculoskeletal diseases (MESH:D009140), functional impairment (MESH:D003072), oncologic (MESH:D000072716), necrosis (MESH:D009336), Duchenne muscular dystrophy (MESH:D020388), myotoxic (MESH:D000081030), ischemia (MESH:D007511), muscular dystrophy (MESH:D009136), -body metabolism (MESH:D008659), crush (MESH:D003444), Muscle trauma (MESH:D019042), vascular occlusion (MESH:D008641), acute injury (MESH:D001930), Crush injury (MESH:D000071576), Fibrosis (MESH:D005355), I/R injuries (MESH:D015427), hematoma (MESH:D006406), long-term functional impairment (MESH:D000088562), battlefield injuries (MESH:D014947), inflammation (MESH:D007249), muscle atrophy (MESH:D009133), X-linked recessive disorder (MESH:D040181), Laceration (MESH:D022125), car accidents (MESH:C566176), /R (MESH:C580424), sports injuries (MESH:D001265), dystrophy (MESH:D058499)
- **Chemicals:** BaCl2 (MESH:C024986), Bupivacaine (MESH:D002045), hyaluronic acid (MESH:D006820), calcium (MESH:D002118), nintedanib (MESH:C530716), AT (MESH:D001246), chondroitin sulfate (MESH:D002809), H&amp;E (MESH:D006371), BioRender (-), polydioxanone (MESH:D016687), picrosirius red (MESH:C009798), nitrogen (MESH:D009584)
- **Species:** Equus caballus (domestic horse, species) [taxon 9796], Ovis aries (domestic sheep, species) [taxon 9940], Oryctolagus cuniculus (domestic rabbit, species) [taxon 9986], Sus scrofa (pig, species) [taxon 9823], Danio rerio (leopard danio, species) [taxon 7955], Felis catus (cat, species) [taxon 9685], Homo sapiens (human, species) [taxon 9606], Canis lupus familiaris (dog, subspecies) [taxon 9615], Mus musculus (house mouse, species) [taxon 10090], Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12938030/full.md

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12938030/full.md

## References

123 references — full list in the complete paper: https://tomesphere.com/paper/PMC12938030/full.md

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Source: https://tomesphere.com/paper/PMC12938030