Heterochronic parabiosis regulates the extent of cellular senescence in multiple tissues
Open accessAbstract
An increase in the burden of senescent cells in tissues with age contributes to driving aging and the onset of age-related diseases. Genetic and pharmacologic elimination of senescent cells extends both health span and life span in mouse models. Heterochronic parabiosis in mice has been used to identify bloodborne, circulating pro- and anti-geronic factors able to drive or slow aging, respectively. However, whether factors in the circulation also regulate senescence is unknown. Here, we measured the expression of senescence and senescence-associated secretory phenotype (SASP) markers in multiple tissues from 4- to 18-month-old male mice that were either isochronically or heterochronically paired for 2 months. In heterochronic parabionts, the age-dependent increase in senescence and SASP marker expression was reduced in old mice exposed to a young environment, while senescence markers were concurrently increased in young heterochronic parabionts. These findings were supported by geropathology analysis using the Geropathology Grading Platform that showed a trend toward reduced hepatic lesions in old heterochronic parabionts. In summary, these results demonstrate that senescence is regulated in part by circulating geronic factors and suggest that one of the possible mediators of the rejuvenating effects with heterochronic parabiosis is through the reduction of the senescent cell burden.
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Blood exchange between young and old mice significantly reduced cellular senescence and SASP marker expression in several aged tissues, while senescence marker levels rose in young animals exposed to old blood.
“Recently, it was reported that blood exchange between young and old mice led to a significant reduction in cellular senescence and SASP marker expression in multiple aged tissues, while at the same time the levels of senescence markers were increased in the young animals exposed to old blood270.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [270]
The SASP disrupts tissue homeostasis by inducing apoptosis or paracrine senescence in neighboring cells, thereby accelerating biological aging.
“The SASP disrupts tissue homeostasis by inducing apoptosis or paracrine senescence in neighboring cells, thereby accelerating the process of biological aging. 52”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [52]
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- Authors
- Yousefzadeh, M. J., Wilkinson, J. E., Hughes, B., Gadela, N., Ladiges, W. C., Vo, N., Niedernhofer, L. J., Huffman, D. M., & Robbins, P. D.
- Affiliations
- University of Minnesota (US)
- University of Washington (US)
- University of Pittsburgh (US)
- Albert Einstein College of Medicine (US)
- Corresponding author
- Huffman, Derek M.
- Robbins, Paul D.
- ORCID
- Venue
- GeroScience
- Published
- 2020-04-13
- Volume
- 42
- Issue
- 3
- Pages
- 951-961
- ISSN
- 2152-4041 (ISSN-L)
- 2509-2715
- 2509-2723
- PMC
- PMC7286998
- OpenAlex
- W3015526708
- Cited by
- 70
- References
- 56
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 10 · 2023: 17 · 2022: 13 · 2021: 8 · 2020: 8
- FWCI
- 6.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- GeroScience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (R21 AG055026, R01 AG044376, U19 AG056278, P30 AG038072)
- American Federation for Aging Research (The Irene Diamond Fund/American Federation on Aging Research Postdoctoral Transition Award)
- National Cancer Institute (P30 CA013330)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- heterochronic parabiosis, cellular senescence, senescence-associated secretory phenotype, aging, age-related diseases, healthspan, lifespan, liver lesions, senolytics
- MeSH terms
- Aging, Animals, Disease Models, Animal, Male, Parabiosis, Biomarkers, Cellular Senescence, Mice
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