STAT3 signaling controls satellite cell expansion and skeletal muscle repair
Open accessAbstract
The progressive loss of muscle regenerative capacity with age or disease results in part from a decline in the number and function of satellite cells, the direct cellular contributors to muscle repair. However, little is known about the molecular effectors underlying satellite cell impairment and depletion. Elevated levels of inflammatory cytokines, including interleukin-6 (IL-6), are associated with both age-related and muscle-wasting conditions. The levels of STAT3, a downstream effector of IL-6, are also elevated with muscle wasting, and STAT3 has been implicated in the regulation of self-renewal and stem cell fate in several tissues. Here we show that IL-6-activated Stat3 signaling regulates satellite cell behavior, promoting myogenic lineage progression through myogenic differentiation 1 (Myod1) regulation. Conditional ablation of Stat3 in Pax7-expressing satellite cells resulted in their increased expansion during regeneration, but compromised myogenic differentiation prevented the contribution of these cells to regenerating myofibers. In contrast, transient Stat3 inhibition promoted satellite cell expansion and enhanced tissue repair in both aged and dystrophic muscle. The effects of STAT3 inhibition on cell fate and proliferation were conserved in human myoblasts. The results of this study indicate that pharmacological manipulation of STAT3 activity can be used to counteract the functional exhaustion of satellite cells in pathological conditions, thereby maintaining the endogenous regenerative response and ameliorating muscle-wasting diseases.
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IL-6 regulates protein homeostasis in skeletal muscle.
“IL‐6 regulates protein homeostasis in the skeletal muscle.”
From Sepsis induces interleukin 6, gp130/JAK2/STAT3, and muscle wasting (2022) · cites this paper as [13]
The Abstract says sustained systemic IL-6 elevation contributes to muscle atrophy, while IL-6 also regulates satellite cell–mediated hypertrophy. That supports a role in skeletal muscle maintenance, but the paper does not establish regulation of protein homeostasis specifically, such as protein synthesis or degradation. (LLM, conf=0.82)
Experimental — accuracy not yet measuredOxidative stress present in the elderly dysregulates typical functions and processes of satellite cells such as proliferation, fibrosis, and differentiation involving Notch, Wnt, p38/MAPK, and JAK-STAT3 signaling pathways.
“In addition, Os present in the elderly dysregulates the typical functions and processes of satellite cells such as proliferation, fibrosis, and differentiation involving Notch, Wnt, p38/MAPK, and the JAK-STAT3 signaling pathways [72, 123–125].”
From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [125]
Aged MuSC dysfunction is attributed to changes in several signal transduction cascades that converge on common cell-cycle kinases and myogenic differentiation factors.
“The cell-intrinsic dysfunction of the aged MuSC population arises from alterations in a combination of multiple signal transduction cascades, which converge on a shared set of cell cycle kinases and myogenic differentiation factors.”
From The central role of muscle stem cells in regenerative failure with aging (2015) · cites this paper as [27]
The changes include cell-autonomous activation of p38α/β MAPK, FGFR-Sprouty1, Jak2-Stat3, and p16Ink4a-Rb pathways.
“These changes include aberrant and cell-autonomous activation of the stress-associated p38α/β mitogen-activated protein kinase (MAPK) signaling axis, the growth factor-stimulated FGFR–Sprouty1 signaling axis, the cytokine-stimulated Jak2–Stat3 signaling axis, and p16Ink4a (also known as Cdkn2a)–Rb cell cycle inhibitors25,27,29,55,56 (Fig. 2).”
From The central role of muscle stem cells in regenerative failure with aging (2015) · cites this paper as [27]
p38α/β MAPK becomes progressively disrupted in aged MuSCs and lies downstream of TNF-α and IL-1.
“Indeed, one of the signaling pathways that is progressively disrupted in aged MuSCs is p38α/β MAPK, which is known to be downstream of TNF-α and IL-1 (refs. 27,56,57).”
From The central role of muscle stem cells in regenerative failure with aging (2015) · cites this paper as [27]
Aged or geriatric MuSCs serially transplanted into young recipients have potent regenerative capacity, whereas rejuvenated MuSCs transplanted into aged or geriatric mice are impaired.
“aged or geriatric MuSCs serially transplanted into young recipients have potent regenerative capacity, whereas rejuvenated MuSCs transplanted into aged or geriatric mice are impaired25,27,29,55,56.”
From The central role of muscle stem cells in regenerative failure with aging (2015) · cites this paper as [27]
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- Authors
- Tierney, M. T., Aydogdu, T., Sala, D., Malecova, B., Gatto, S., Puri, P. L., Latella, L., & Sacco, A.
- Affiliations
- Sanford Burnham Prebys Medical Discovery Institute (US)
- Istituto di Farmacologia Traslazionale (IT)
- Corresponding author
- Sacco, Alessandra
- Venue
- Nature Medicine
- Published
- 2014-09-07
- Volume
- 20
- Issue
- 10
- Pages
- 1182-1186
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC4332844
- OpenAlex
- W2047018308
- Cited by
- 401
- References
- 44
- Citations by year
- 2026: 27 · 2025: 32 · 2024: 25 · 2023: 21 · 2022: 30 · 2021: 32 · 2020: 39 · 2019: 35 · 2018: 34 · 2017: 40 · 2016: 42 · 2015: 38 · 2014: 6
- FWCI
- 17.23
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (F31AR065923, R01AR052779, R01AR064873, P30AR061303, R03AR063328, R01AR056712)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Genetics › Neurogenetic and Muscular Disorders Research
- Keywords
- STAT3 signaling, satellite cells, skeletal muscle regeneration, interleukin-6, MyoD, myogenesis, Pax7, muscle atrophy, dystrophic muscle, aging, muscle regeneration, stem cell self-renewal
- MeSH terms
- Aging, Animals, Cells, Cultured, Humans, Male, Mice, Inbred C57BL, Regeneration, Signal Transduction, MyoD Protein, Mice, Inbred mdx, Mice, Knockout, Muscle Development, Satellite Cells, Skeletal Muscle, Cell Proliferation, STAT3 Transcription Factor, Mice, PAX7 Transcription Factor
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