TGF-β Signaling in Cellular Senescence and Aging-Related Pathology
Open accessAbstract
Aging is broadly defined as the functional decline that occurs in all body systems. The accumulation of senescent cells is considered a hallmark of aging and thought to contribute to the aging pathologies. Transforming growth factor-β (TGF-β) is a pleiotropic cytokine that regulates a myriad of cellular processes and has important roles in embryonic development, physiological tissue homeostasis, and various pathological conditions. TGF-β exerts potent growth inhibitory activities in various cell types, and multiple growth regulatory mechanisms have reportedly been linked to the phenotypes of cellular senescence and stem cell aging in previous studies. In addition, accumulated evidence has indicated a multifaceted association between TGF-β signaling and aging-associated disorders, including Alzheimer’s disease, muscle atrophy, and obesity. The findings regarding these diseases suggest that the impairment of TGF-β signaling in certain cell types and the upregulation of TGF-β ligands contribute to cell degeneration, tissue fibrosis, inflammation, decreased regeneration capacity, and metabolic malfunction. While the biological roles of TGF-β depend highly on cell types and cellular contexts, aging-associated changes are an important additional context which warrants further investigation to better understand the involvement in various diseases and develop therapeutic options. The present review summarizes the relationships between TGF-β signaling and cellular senescence, stem cell aging, and aging-related diseases.
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TGF-β participates in multiple signaling pathways and has broad, context-dependent effects.
“Moreover, TGF-β participates in multiple signaling pathways and has broad, context-dependent effects [14].”
From Ensemble of Time-Evolving SASP Gene Sets Identifies IGFBP7 and CDKN1A as a Potential Marker Pair for Senescent Fibroblast Subpopulations Across Tissues (2026) · cites this paper as [14]
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- Authors
- Tominaga, K., & Suzuki, H. I.
- Affiliations
- Massachusetts Institute of Technology (US)
- Koch Institute for Integrative Cancer Research At MIT (US)
- Corresponding author
- Suzuki, Hiroshi I.
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2019-10-10
- Volume
- 20
- Issue
- 20
- Pages
- 5002
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC6834140
- OpenAlex
- W2979971613
- Cited by
- 393
- References
- 139
- Citations by year
- 2026: 54 · 2025: 84 · 2024: 82 · 2023: 56 · 2022: 51 · 2021: 47 · 2020: 19
- FWCI
- 2.58
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Grant-in-Aid for JSPS postdoc Fellows (NA)
- the Osamu Hayaishi Memorial Scholarship for Study Abroad (NA)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- TGF-beta signaling, cellular senescence, aging, stem cell aging, age-related diseases, Alzheimer's disease, muscle atrophy, obesity, fibrosis, inflammation, tissue regeneration, metabolic dysfunction
- MeSH terms
- Aging, Alzheimer Disease, Fibrosis, Hematopoietic Stem Cells, Homeostasis, Inflammation, Ligands, Muscular Atrophy, Obesity, Stem Cells, Signal Transduction, Transforming Growth Factor beta, Cellular Senescence, Cell Proliferation, Mesenchymal Stem Cells
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