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Peer-reviewedCC BY-NC-NDStem Cell Reports

Resident mesenchymal progenitor cells require autocrine IGF-I in homeostatic and regenerating skeletal muscle

  • Yangyi E. Luo1
  • Zoe Abe-Teh2
  • Tarek Y. Alsaghir2
  • Li-Ying Kuo2
  • Fahong Yu3
  • Bradley E. Stoker2
  • Yumei Zhou4
  • Ambili Bai Appu5
  • Elijah M. Dy2
  • Feng Yue6
  • Daniel Kopinke7
  • Elisabeth R. Barton8
8 affiliations
  1. 1Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL, USA; Myology Institute, University of Florida, Gainesville, FL, USA
  2. 2Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL, USA
  3. 3Interdisciplinary Center for Biotechnology Research, University of Florida, Gainesville, FL, USA
  4. 4Department of Animal Sciences, University of Florida, Gainesville, FL, USA
  5. 5Department of Pharmacology and Therapeutics, University of Florida, Gainesville, FL, USA
  6. 6Myology Institute, University of Florida, Gainesville, FL, USA; Department of Animal Sciences, University of Florida, Gainesville, FL, USA
  7. 7Department of Pharmacology and Therapeutics, University of Florida, Gainesville, FL, USA; Myology Institute, University of Florida, Gainesville, FL, USA
  8. 8Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL, USA; Myology Institute, University of Florida, Gainesville, FL, USA. Electronic address: [email protected]
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Abstract

Fibro-adipogenic progenitors (FAPs) are muscle-resident mesenchymal stromal cells essential for homeostasis and regeneration but can produce fibrosis or intramuscular fat in pathological conditions. Insulin-like growth factor-I (IGF-I) regulates regeneration through actions on muscle fibers, satellite cells, macrophages, and extracellular matrix (ECM) remodeling but has multiple sources. To assess the role of FAP-derived IGF-I, we generated inducible FAP-specific Igf1 -deficient (FID) mice. Following BaCl 2 injury, FID muscles displayed impaired regeneration, with smaller fibers, fewer Pax7 + and MyoD + cells, increased CD68 + macrophages, decreased collagen, and suppressed FAP proliferation. After glycerol-induced injury, FID muscles had reduced fat. Primary FID FAPs displayed blunted proliferation, upregulated immune-regulatory genes, and downregulated ECM and growth genes, with delayed fibrogenic and adipogenic differentiation. scRNA-seq of homeostatic muscle revealed reduced protein translation and ECM indices alongside increased senescence markers in FID samples. Taken together, FAP IGF-I is critical for FAP function, with direct and indirect impact on muscle regeneration.

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Cite

BibTeXRIS
BibTeX
@article{luo2026resident,
  title = {{Resident mesenchymal progenitor cells require autocrine IGF-I in homeostatic and regenerating skeletal muscle}},
  author = {Yangyi E. Luo and Zoe Abe-Teh and Tarek Y. Alsaghir and Li-Ying Kuo and Fahong Yu and Bradley E. Stoker and Yumei Zhou and Ambili Bai Appu and Elijah M. Dy and Feng Yue and Daniel Kopinke and Elisabeth R. Barton},
  journal = {Stem Cell Reports},
  year = {2026},
  month = jun,
  doi = {10.1016/j.stemcr.2026.102973},
  url = {https://doi.org/10.1016/j.stemcr.2026.102973},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Resident mesenchymal progenitor cells require autocrine IGF-I in homeostatic and regenerating skeletal muscle
AU  - Yangyi E. Luo
AU  - Zoe Abe-Teh
AU  - Tarek Y. Alsaghir
AU  - Li-Ying Kuo
AU  - Fahong Yu
AU  - Bradley E. Stoker
AU  - Yumei Zhou
AU  - Ambili Bai Appu
AU  - Elijah M. Dy
AU  - Feng Yue
AU  - Daniel Kopinke
AU  - Elisabeth R. Barton
PY  - 2026
DA  - 2026/06/25
JO  - Stem Cell Reports
DO  - 10.1016/j.stemcr.2026.102973
UR  - https://doi.org/10.1016/j.stemcr.2026.102973
AB  - Fibro-adipogenic progenitors (FAPs) are muscle-resident mesenchymal stromal cells essential for homeostasis and regeneration but can produce fibrosis or intramuscular fat in pathological conditions. Insulin-like growth factor-I (IGF-I) regulates regeneration through actions on muscle fibers, satellite cells, macrophages, and extracellular matrix (ECM) remodeling but has multiple sources. To assess the role of FAP-derived IGF-I, we generated inducible FAP-specific Igf1 -deficient (FID) mice. Following BaCl 2 injury, FID muscles displayed impaired regeneration, with smaller fibers, fewer Pax7 + and MyoD + cells, increased CD68 + macrophages, decreased collagen, and suppressed FAP proliferation. After glycerol-induced injury, FID muscles had reduced fat. Primary FID FAPs displayed blunted proliferation, upregulated immune-regulatory genes, and downregulated ECM and growth genes, with delayed fibrogenic and adipogenic differentiation. scRNA-seq of homeostatic muscle revealed reduced protein translation and ECM indices alongside increased senescence markers in FID samples. Taken together, FAP IGF-I is critical for FAP function, with direct and indirect impact on muscle regeneration.
SN  - 2213-6711
ER  -