Mesenchymal stem cell‐derived extracellular vesicles reduce senescence and extend health span in mouse models of aging
Open accessAbstract
Aging drives progressive loss of the ability of tissues to recover from stress, partly through loss of somatic stem cell function and increased senescent burden. We demonstrate that bone marrow‐derived mesenchymal stem cells (BM‐MSCs) rapidly senescence and become dysfunctional in culture. Injection of BM‐MSCs from young mice prolonged life span and health span, and conditioned media (CM) from young BM‐MSCs rescued the function of aged stem cells and senescent fibroblasts. Extracellular vesicles (EVs) from young BM‐MSC CM extended life span of Ercc1 −/− mice similarly to injection of young BM‐MSCs. Finally, treatment with EVs from MSCs generated from human ES cells reduced senescence in culture and in vivo , and improved health span. Thus, MSC EVs represent an effective and safe approach for conferring the therapeutic effects of adult stem cells, avoiding the risks of tumor development and donor cell rejection. These results demonstrate that MSC‐derived EVs are highly effective senotherapeutics, slowing the progression of aging, and diseases driven by cellular senescence.
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Many studies have shown that the number and function of different somatic cell populations declines with age, which diminishes the regenerative potential of tissues and organs.
“Many studies have shown that the number and function of different somatic cell populations declines with age, which diminishes the regenerative potential of tissues and organs.”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [355]
The Discussion says that numerous studies suggest the number and function of diverse somatic stem-cell populations decline with age. The Introduction links loss of regenerative capacity to declining functional adult stem cells as a hypothesis, while the Discussion notes limited evidence that stem-cell loss is a primary driver of age-related pathology. The claim broadens stem cells to somatic cells generally and states the regenerative consequence more definitively than the source does. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThere is limited evidence that loss of stem cell function is a major driver of age-related pathology and shortened lifespan.
“However, there is limited evidence that loss of stem cell function is a major driver of age-related pathology and shortened lifespan.355–358”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [355]
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References 45 · Cited by 153
Research works printed but not linked: 1
- Fuhrmann‐Stroissnigg, H., Ling, Y. Y., Zhao, J., McGowan, S. J., Zhu, Y. I., Brooks, R. W., Grassi, D., Gregg, S. Q., Stripay, J. L., Dorronsoro, A., Corbo, L., Tang, P., Bukata, C., Ring, N., Giacca, M, Li, X., Tchkonia, T., Kirkland, J. L., Niedernhofer, L. J., Robbins, P. D. (2017). Identification of HSP90 inhibitors as a novel class of senolytics. Nature Communications, 8, 422. 10.1038/s41467-017-00314-z PMC5583353 28871086 · DOI · Paper page
- Authors
- Dorronsoro, A., Santiago, F. E., Grassi, D., Zhang, T., Lai, R. C., McGowan, S. J., Angelini, L., Lavasani, M., Corbo, L., Lu, A., Brooks, R. W., Garcia‐Contreras, M., Stolz, D. B., Amelio, A., Boregowda, S. V., Fallahi, M., Reich, A., Ricordi, C., Phinney, D. G., Huard, J., Lim, S. K., Niedernhofer, L. J., & Robbins, P. D.
- Affiliations
- Center on Aging and Departments of Molecular Medicine Scripps Research Jupiter Florida USA
- University of Minnesota (US)
- Agency for Science, Technology and Research (SG)
- Shirley Ryan AbilityLab (US)
- Steadman Philippon Research Institute (US)
- Diabetes Research Institute University of Miami Miami Florida USA
- University of Pittsburgh (US)
- University of North Carolina at Chapel Hill (US)
- University of Miami (US)
- Corresponding author
- Robbins, Paul D.
- ORCID
- Dorronsoro, Akaitz
- Santiago, Fernando E.
- Grassi, Diego
- Zhang, Tianpeng
- Lai, Ruenn Chai
- McGowan, Sara J.
- Lavasani, Mitra
- Lu, Aiping
- Stolz, Donna B.
- Amelio, Antonio
- Boregowda, Siddaraju V.
- Fallahi, Mohammad
- Reich, Adrian
- Ricordi, Camillo
- Phinney, Donald G.
- Huard, Johnny
- Lim, Sai Kiang
- Niedernhofer, Laura J.
- Robbins, Paul D.
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2021-03-16
- Volume
- 20
- Issue
- 4
- Pages
- e13337-e13337
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC8045949
- OpenAlex
- W3136146286
- Cited by
- 153
- References
- 45
- Citations by year
- 2026: 22 · 2025: 35 · 2024: 34 · 2023: 32 · 2022: 16 · 2021: 14
- FWCI
- 15.06
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Aging Cell (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (P01AG062412, PO1AG043376, R01AG063543, R56AG4059675, RO1AR065445, U19AG056278)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Extracellular vesicles in disease
- Keywords
- mesenchymal stem cells, extracellular vesicles, cellular senescence, healthspan, aging, senotherapeutics, bone marrow-derived stem cells, stem cell rejuvenation, conditioned medium, fibroblast senescence, lifespan extension
- MeSH terms
- Human Embryonic Stem Cells, Extracellular Vesicles, Senotherapeutics, Aging, Animals, DNA-Binding Proteins, Endonucleases, Fibroblasts, Humans, Longevity, Mice, Inbred C57BL, Signal Transduction, Cellular Senescence, Culture Media, Conditioned, Mice, Knockout, Models, Animal, Mice, Mesenchymal Stem Cells
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