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An aged immune system drives senescence and ageing of solid organs
Open accessAbstract
Ageing of the immune system, or immunosenescence, contributes to the morbidity and mortality of the elderly 1,2. To define the contribution of immune system ageing to organism ageing, here we selectively deleted Ercc1, which encodes a crucial DNA repair protein 3,4, in mouse haematopoietic cells to increase the burden of endogenous DNA damage and thereby senescence 5-7 in the immune system only. We show that Vav-iCre+/-;Ercc1-/fl mice were healthy into adulthood, then displayed premature onset of immunosenescence characterized by attrition and senescence of specific immune cell populations and impaired immune function, similar to changes that occur during ageing in wild-type mice 8-10. Notably, non-lymphoid organs also showed increased senescence and damage, which suggests that senescent, aged immune cells can promote systemic ageing. The transplantation of splenocytes from Vav-iCre+/-;Ercc1-/fl or aged wild-type mice into young mice induced senescence in trans, whereas the transplantation of young immune cells attenuated senescence. The treatment of Vav-iCre+/-;Ercc1-/fl mice with rapamycin reduced markers of senescence in immune cells and improved immune function 11,12. These data demonstrate that an aged, senescent immune system has a causal role in driving systemic ageing and therefore represents a key therapeutic target to extend healthy ageing.
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“Once senescent cell burden surpasses this threshold, continuing increases in proapoptotic/pro-inflammatory senescent cell burden may contribute to tissue destruction and hence development or progression of multiple diseases and age-related disorders (Table 2) as well as immune dysregulation, further amplifying senescent cell accumulation in a feed-forward loop36,38,62.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [38]
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“The senescent cell fate can be triggered by a number of stressors including DNA damage, cancerous mutations or oncogene activation, mitochondrial dysfunction, reactive metabolites, hyperoxia or hypoxia, proteotoxic stress, extracellular signals, infections, mechanical or shear stresses that deform cells, resistance exercise and factors secreted by other senescent cells18,38–47.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [38]
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“Mouse models of rapid telomere shortening, dysfunctional mitosis or impaired DNA repair (Terc, BubR1, and Ercc1 mutant mice, respectively), display high levels of cellular senescence and accelerated aging86,99,100.”
From Guidelines for minimal information on cellular senescence experimentation in vivo (2024) · cites this paper as [99]
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In the citing paper
“CD3+ T cells isolated from the blood of aged mice and of mice deficient in ERCC1, which is a crucial DNA repair protein, exhibit increased levels of multiple senescent markers, including Ccl2, Tnf, Il1b, Inhba, Spp1, Cdkn2a and Cdkn1a (refs. 85,86).”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [86]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“As a result of the effects of cellular senescence, chronic inflammation, and immunosenescence, the pathological aging of organs increases the level of inflammation and makes repair difficult, ultimately leading to diseases.10”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [10]
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“In aging tissues, molecular and cellular changes disrupt spatial organization, resulting in uneven functional decline.”
From Spatial transcriptomic landscape unveils immunoglobin-associated senescence as a hallmark of aging (2024) · cites this paper as [5]
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“These and other models, for which it has been shown that accelerated aging depends, at least partly, on cellular senescence, are valuable for studying the impact of senescence on health and lifespan”
From Guidelines for minimal information on cellular senescence experimentation in vivo (2024) · cites this paper as [99]
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In the citing paper
“Furthermore, the functionally weakened immune system in old age44 does not clear senescent cells, which may account for their persistence in damaged aged muscle; this exacerbates tissue regenerative impairment.”
From Senescence atlas reveals an aged-like inflamed niche that blunts muscle regeneration (2023) · cites this paper as [44]
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“Premature aging of the immune system has been shown to drive aging of multiple other organ systems in mice 81.”
From Targeting the biology of aging with mTOR inhibitors (2023) · cites this paper as [81]
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In the citing paper
“Notably, clearing senescent cells in peripheral tissues may also positively impact the brain55.”
From Senolytic therapy in mild Alzheimer's disease: a phase 1 feasibility trial (2023) · cites this paper as [55]
Experimental — accuracy not yet measuredIn the citing paper
“suggesting that a senescent immune system contributes to aging phenotypic features in immune cells and in solid, nonlymphoid tissues.”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [26]
In the citing paper
“Deletion of ERCC1, a crucial DNA repair protein, in mouse hematopoietic cells leads to accelerated senescence of the immune system.”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [26]
In the citing paper
“Accordingly, mice lacking ERCC1 in hematopoietic cells, as well as aged mice, express elevated markers of senescence (p16, p21) in many immune cells with concomitant impairment of immune function.”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [26]
In the citing paper
“Strikingly, transfer of splenocytes from aged wild-type mice or mice lacking ERCC1 into young animals increased the senescence burden in nonlymphoid organs, suggesting that a senescent immune system contributes to aging phenotypic features in immune cells and in solid, nonlymphoid tissues.”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [26]
In the citing paper
“Notably, the selective induction of immune cell ageing increases the levels of the ageing markers p16 and p21 in multiple organs, including the brain,328 thereby highlighting the crucial roles played by the immune system in the process of ageing.”
From Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances (2025) · cites this paper as [328]
In the citing paper
“Immunosenescence is characterized by dysfunctions in monocyte and neutrophil phagocytosis, decreased numbers of naive T cells, increased numbers of memory T cells,327 and increased SASP secretion by these cells,327,328 thereby weakening the immune response to foreign antigens.”
From Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances (2025) · cites this paper as [328]
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“Created using Biorender.com. throughout the body, leading to early mortality (Yousefzadeh et al., 2021).”
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Sun, P.-Y., Liu, J., Hu, J.-N., Tu, Y.-F., Jiang, Q., Jia, Y.-J., Sun, H.-L., Chen, S.-H., Xin, J.-Y., Yu, Z.-Y., et al. (2024) · Science Advances · doi:10.1126/sciadv.adl1123 · Cited by 46
Self-citationIFN-Aging: Coupling Aging With Interferon Response
Cao, W. (2022) · Frontiers in Aging · doi:10.3389/fragi.2022.870489 · Cited by 44
Neutrophils in homeostasis and tissue repair
Shim, H. B., Deniset, J., & Kubes, P. (2022) · International Immunology · doi:10.1093/intimm/dxac029 · Cited by 46
The immunopathology of B lymphocytes during stroke-induced injury and repair
Malone, M. K., Ujas, T. A., Britsch, D. R. S., Cotter, K. M., Poinsatte, K., & Stowe, A. M. (2022) · Seminars in Immunopathology · doi:10.1007/s00281-022-00971-3 · Cited by 45
“The humoral immune system is subjected to this same process, which may result in immunosenescence [55], or the increasing inability for immune cells to respond to infection or other stimuli [21, 96].”
BackgroundDifferences in the post-stroke innate immune response between young and old
Gallizioli, M., Arbaizar‐Rovirosa, M., Brea, D., & Planas, A. M. (2023) · Seminars in Immunopathology · doi:10.1007/s00281-023-00990-8 · Cited by 45
“Importantly, several lines of evidence suggest that the peripheral immune system and blood factors of the elderly contribute to age-dependent cognitive decline [56, 57] and exacerbate the stroke brain lesion [58].”
BackgroundTai, G., Ma, Y.-J., Feng, J.-L., Li, J., Qiu, S., Yu, Q., Liu, R.-H., Silumbwe, C. W., Wang, X., Li, X., et al. (2024) · Cardiovascular Research · doi:10.1093/cvr/cvae079 · Cited by 44
Cellular senescence in cancer: molecular mechanisms and therapeutic targets
Jin, P., Duan, X., Li, L., Zhou, P., Zou, C., & Xie, K. (2024) · MedComm · doi:10.1002/mco2.542 · Cited by 51
“279 For instance, research suggests that the pathophysiology and management of individuals with breast cancer are pro-foundly influenced by immunosenescence, particularly CD8 + T-cell senescence.”
BackgroundInfluentialTrussoni, C. E., O’Hara, S. P., & LaRusso, N. F. (2022) · Seminars in Immunopathology · doi:10.1007/s00281-022-00909-9 · Cited by 44
“Here, the authors showed that immunosenescence led to impaired immune function and systemic premature aging [27].”
BackgroundSelf-citationInfluential factors of saliva microbiota composition
Wells, P. M., Sprockett, D. D., Bowyer, R. C. E., Kurushima, Y., Relman, D. A., Williams, F. M. K., & Steves, C. J. (2022) · Scientific Reports · doi:10.1038/s41598-022-23266-x · Cited by 43
Han, J. J. (2023) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2023.09.007 · Cited by 45
Systemic aging and aging‐related diseases
Li, Q., Xiao, N., Zhang, H., Liang, G., Lin, Y., Qian, Z., Yang, X. Y., Yang, J., Fu, Y., Zhang, C., et al. (2025) · The FASEB Journal · doi:10.1096/fj.202402479rrr · Cited by 45
“43 Transplantation of aged immune cells to young mice accelerated the aging of young mice; on the other hand, young immune cells alleviated the senescent phenotype of aged mice.”
InfluentialMore TOR: The expanding role of mTOR in regulating immune responses
Patel, C. H., & Powell, J. D. (2025) · Immunity · doi:10.1016/j.immuni.2025.06.010 · Cited by 48
Immune surveillance of senescent cells in aging and disease
Majewska, J., & Krizhanovsky, V. (2025) · Nature Aging · doi:10.1038/s43587-025-00910-5 · Cited by 50
“As the accumulation of senescent cells and the recruitment of immune cells that become dysfunctional with age are intimately linked 15,66,76–78 , targeting age-related chronic inflammation is a promising direct antiaging strategy with the potential to limit the senescent cell burden.”
InfluentialCD11bhigh B Cells Increase after Stroke and Regulate Microglia
Korf, J. M., Honarpisheh, P., Mohan, E. C., Banerjee, A., Blasco-Conesa, M. P., Honarpisheh, P., Guzman, G. U., Khan, R., Ganesh, B. P., Hazen, A. L., et al. (2022) · The Journal of Immunology · doi:10.4049/jimmunol.2100884 · Cited by 44
Clonal haematopoiesis, ageing and kidney disease
Vlasschaert, C., Lanktree, M. B., Rauh, M. J., Kelly, T. N., & Natarajan, P. (2023) · Nature Reviews Nephrology · doi:10.1038/s41581-023-00778-x · Cited by 42
Zheng, L., He, S., Wang, H., Li, J., Liu, Y., & Liu, S. (2024) · Aging and Disease · doi:10.14336/ad.2024.0206 · Cited by 46
“Transplantation of senescent immune cells can also promote senescence and tissue damage [62].”
InfluentialActivatable senoprobes and senolytics: Novel strategies to detect and target senescent cells
Morsli, S., Doherty, G. J., & Muñoz‐Espín, D. (2022) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2021.111618 · Cited by 41
Bhattacharya, K., Maiti, S., Zahoran, S., Weidenauer, L., Hany, D., Wider, D., Bernasconi, L., Quadroni, M., Collart, M., & Picard, D. (2022) · Nature Communications · doi:10.1038/s41467-022-33916-3 · Cited by 40
Liu, C., Liao, W., Chen, J., Yu, K., Wu, Y., Zhang, S., Chen, M., Chen, F., Wang, S., Cheng, T., et al. (2023) · Redox Biology · doi:10.1016/j.redox.2023.102661 · Cited by 46
The multifaceted role of macrophages in homeostatic and injured skeletal muscle
Wang, X., & Zhou, L. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1274816 · Cited by 45
“Aging results in a plethora of phenotypic and functional changes in macrophages, including but not limited to the increased production of pro-in fl ammatory mediators such as TNF-a and IL-1 b and decreased capacity of phagocytosis (170, 172).”
BackgroundMethodOrtega-Molina, A., Lebrero‐Fernández, C., Sanz, A., Calvo‐Rubio, M., Deleyto-Seldas, N., de Prado-Rivas, L., Plata-Gómez, A. B., Fernández-Florido, E., González‐García, P., Vivas, Y., et al. (2024) · Nature Aging · doi:10.1038/s43587-024-00635-x · Cited by 45
“Myeloid inflammation can be detrimental for organ homeostasis 53,54 , so to test whether Rragc S74N/+ neutrophils were cell-intrinsically dysfunctional and potential drivers of the health decline of Rragc S74N/+ mice, we purified BM-derived neutrophils from Rragc +/+ and Rragc S74N/+ mice and…”
Recent Advances in Aging and Immunosenescence: Mechanisms and Therapeutic Strategies
Wang, S., Huo, T., Lu, M., Zhao, Y., Zhang, J., He, W., & Chen, H. (2025) · Cells · doi:10.3390/cells14070499 · Cited by 47
“However, senescent immune cells not only fail to clear SCs and inflammatory factors but also accelerate the aging of the body, thereby forming a vicious cycle of inflammation and aging [33].”
InfluentialMitochondrial dysfunction in cellular senescence: a bridge to neurodegenerative disease
Hruby, A. J., & Higuchi‐Sanabria, R. (2025) · npj Aging · doi:10.1038/s41514-025-00291-4 · Cited by 52
Bai, Z., Yang, P., Yu, F., Li, Z., Yao, Z., Martinez, J., Li, M., & Xu, H. (2022) · Cell Death & Disease · doi:10.1038/s41419-022-04562-w · Cited by 43
“However, with increasing age, the efficiency of the immune system decreases, which can lead to the immune escape of SNCs [18].”
BackgroundThe diseased kidney: aging and senescent immunology
Chi, M., Tian, Z., Ma, K., Li, Y., Wang, L., Nasser, M. I., & Liu, C. (2022) · Immunity & Ageing · doi:10.1186/s12979-022-00313-9 · Cited by 43
“In other words, the immune response is age dependent [2].”
BackgroundLack of evidence for increased transcriptional noise in aged tissues
Ibáñez-Solé, O., Ascensión, A. M., Araúzo-Bravo, M. J., & Izeta, A. (2022) · eLife · doi:10.7554/elife.80380 · Cited by 38
Li, N., Ye, Y., Wu, Y., Li, L., Hu, J., Luo, D., Li, Y., Yang, J., Gao, Y., Hai, W., et al. (2023) · iScience · doi:10.1016/j.isci.2023.106571 · Cited by 44
The foreign body response: emerging cell types and considerations for targeted therapeutics
Yang, B., Rutkowski, N., & Elisseeff, J. H. (2023) · Biomaterials Science · doi:10.1039/d3bm00629h · Cited by 44
The Role of Ageing and Parenchymal Senescence on Macrophage Function and Fibrosis
Campbell, R., Docherty, M.-H., Ferenbach, D. A., & Mylonas, K. J. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.700790 · Cited by 41
“Recent research has provided more evidence for senescent macrophages, as shown by significant upregulation of both p16 and p21 cell-cycle checkpoints in a mouse model of DNA damage repair deficiency (129).”
BackgroundSoluble factors influencing the neural stem cell niche in brain physiology, inflammation, and aging
Willis, C. M., Nicaise, A. M., Krzak, G., Ionescu, R.-B., Pappa, V., D’Angelo, A., Agarwal, R., Repollés-de-Dalmau, M., Peruzzotti‐Jametti, L., & Pluchino, S. (2022) · Experimental Neurology · doi:10.1016/j.expneurol.2022.114124 · Cited by 43
“Aging of the immune system, known as immunosenescence, has been found to contribute to whole body aging, including expression of increased aging markers, such as p16, a cell cycle inhibitor, in the brain (143).”
BackgroundAging disrupts MANF-mediated immune modulation during skeletal muscle regeneration
Sousa, N. S., Brás, M. F., Antunes, I. B., Lindholm, P., Neves, J., & Sousa‐Victor, P. (2023) · Nature Aging · doi:10.1038/s43587-023-00382-5 · Cited by 40
Immunometabolism and oxidative stress: roles and therapeutic strategies in cancer and aging
Zhou, N.-J., Bao, W.-Q., Zhang, C., Jiang, M., Liang, T.-L., Ma, G.-Y., Liu, L., Pan, H., & Li, R.-Z. (2025) · npj Aging · doi:10.1038/s41514-025-00250-z · Cited by 45
“This decline includes altered ratios of naive to memory T cells, disruptions in the CD4/CD8 balance, impaired calcium signaling, and thymic involution 40 .”
The Molecular and Cellular Basis of Hutchinson–Gilford Progeria Syndrome and Potential Treatments
Batista, N. J., Desai, S. G., Perez, A. M., Finkelstein, A., Radigan, R., Singh, M., Landman, A., Drittel, B., Abramov, D., Ahsan, M., et al. (2023) · Genes · doi:10.3390/genes14030602 · Cited by 45
“In normal aging, DNA damage is a prominently observed phenotype due to both exogenous and endogenous sources of damage [66,67,76].”
BackgroundAlveolar epithelial regeneration in the aging lung
Han, S., Budinger, G. R. S., & Gottardi, C. J. (2023) · Journal of Clinical Investigation · doi:10.1172/jci170504 · Cited by 40
“These include the accumulation of DNA damage with age (168), the loss of transcriptional fidelity leading to a length imbalance favoring long transcripts in the transcriptome (169), and telomere shortening, the effects of which have been localized to the alveolar epithelium in animal models (97,…”
The central role of DNA damage in immunosenescence
Kell, L., Simon, A. K., Alsaleh, G., & Cox, L. S. (2023) · Frontiers in Aging · doi:10.3389/fragi.2023.1202152 · Cited by 44
Cheng, X., Jiang, S., Pan, B., Xie, W., & Meng, J. (2023) · Lipids in Health and Disease · doi:10.1186/s12944-023-01964-3 · Cited by 40
“There was a twofold increase in CD3 + T cells, predominantly CD8 + T cells (cytotoxic T cells), in aged mouse VAT compared to young animal VAT, and a similar trend was observed in obese mice [66, 67].”
BackgroundNatural killer cells in the central nervous system
Ning, Z., Liu, Y., Guo, D., Lin, W., & Tang, Y. (2023) · Cell Communication and Signaling · doi:10.1186/s12964-023-01324-9 · Cited by 41
“Interestingly, an aged immune system drives senescent phenotypes in non-lymphoid tissues including the brain, suggesting brain aging might be affected by the dysfunctional immune system [107].”
BackgroundT cell senescence: a new perspective on immunotherapy in lung cancer
Huang, M., Wang, Y., Fang, L., Liu, C., Feng, F., Liu, L., & Sun, C. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1338680 · Cited by 37
Self-citationTo target cellular senescence in diabetic kidney disease: the known and the unknown
Wei, Y., Mou, S., Yang, Q., Liu, F., Cooper, M. E., & Chai, Z. (2024) · Clinical Science · doi:10.1042/cs20240717 · Cited by 41
“Increased deposition of γ H2AX has been widely used as a marker of DDR or a genotoxic stress marker in research [62,63].”
BackgroundIL-23R is a senescence-linked circulating and tissue biomarker of aging
Carver, C. M., Rodriguez, S. L., Atkinson, E. J., Dosch, A. J., Asmussen, N. C., Gomez, P. T., Leitschuh, E. A., Espíndola‐Netto, J. M., Jeganathan, K. B., Whaley, M. G., et al. (2024) · Nature Aging · doi:10.1038/s43587-024-00752-7 · Cited by 40
An overview of contemporary theories of ageing
de Magalhães, J. P. (2025) · Nature Cell Biology · doi:10.1038/s41556-025-01698-7 · Cited by 47
“Genetic manipulations in mice that cause premature loss of immune function with age, termed immunosenescence, also accelerate age-related decline and shorten lifespan 69,70 .”
A geroscience motivated approach to treat Alzheimer’s disease: Senolytics move to clinical trials
Gonzales, M. M., Krishnamurthy, S., Garbarino, V. R., Daeihagh, A. S., Gillispie, G. J., Deep, G., Craft, S., & Orr, M. E. (2021) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2021.111589 · Cited by 37
Cellular Senescence in Immunity against Infections
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“The selective deletion of Ercc1, encoding a crucial DNA repair protein in mouse hematopoietic cells, resulted in the accumulation of spontaneous DNA damage and the premature onset of immunosenescence in mice, which was associated with increased levels of cellular senescence and damage in non-lymphoid organs [17].”
BackgroundRecent insights into the crosstalk between senescent cells and CD8 T lymphocytes
Marín, I., Serrano, M., & Pietrocola, F. (2023) · npj Aging · doi:10.1038/s41514-023-00105-5 · Cited by 41
Age-associated changes in innate and adaptive immunity: role of the gut microbiota
Gao, H., Nepovimová, E., Adam, V., Heger, Z., Valko, M., Wu, Q., & Kuča, K. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1421062 · Cited by 41
“Subsequent in vivo animal experiments have conclusively demonstrated that senescent immune cells can induce systemic tissue damage and lead to a shortened lifespan (309).”
BackgroundChen, Y., Xie, K., Han, Y., Xu, Q., & Zhao, X. (2023) · Journal of Inflammation Research · doi:10.2147/jir.s427149 · Cited by 35
Transplanting old organs promotes senescence in young recipients
Iske, J., Roesel, M. J., Martin, F., Schroeter, A., Matsunaga, T., Maenosono, R., Tripathi, U., Xiao, Y., Nian, Y., Caldarone, B. J., et al. (2023) · American Journal of Transplantation · doi:10.1016/j.ajt.2023.10.013 · Cited by 35
Conway, J., Jong, E. N. D., White, A. J., Dugan, B., Rees, N. P., Parnell, S. M., Lamberte, L. E., Sharma‐Oates, A., Sullivan, J., Mauro, C., et al. (2024) · Aging Cell · doi:10.1111/acel.14401 · Cited by 41
Enhancing immunity during ageing by targeting interactions within the tissue environment
Bracken, O. V., Maeyer, R. P. H. D., & Akbar, A. N. (2025) · Nature Reviews Drug Discovery · doi:10.1038/s41573-024-01126-9 · Cited by 43
“One of the most profound cellular changes during ageing is cellular senescence, whereby cells enter a stable state of cell cycle arrest 4 resulting from stress responses, cumulative DNA damage, nutritional deprivation or telomere erosion owing to repeated cell division 5–9 .”
Metadata
- Authors
- Yousefzadeh, M. J., Flores, R. R., Zhu, Y., Schmiechen, Z. C., Brooks, R. W., Trussoni, C. E., Cui, Y., Angelini, L., Lee, K.-A., McGowan, S. J., Burrack, A. L., Wang, D., Dong, Q., Lu, A., Sano, T., O’Kelly, R. D., McGuckian, C. A., Kato, J. I., Bank, M. P., Wade, E. A., Pillai, S. P. S., Klug, J., Ladiges, W. C., Burd, C. E., Lewis, S. E., LaRusso, N. F., Vo, N. V., Wang, Y., Kelley, E. E., Huard, J., Stromnes, I. M., Robbins, P. D., & Niedernhofer, L. J.
- Affiliations
- University of Minnesota (US)
- Mayo Clinic (US)
- Scripps Research Institute (US)
- University of California, Riverside (US)
- University of Pittsburgh (US)
- The University of Texas Health Science Center at Houston (US)
- Fred Hutch Cancer Center (US)
- University of Washington (US)
- The Ohio State University (US)
- West Virginia University (US)
- Corresponding author
- Robbins, Paul D.
- Niedernhofer, Laura J.
- ORCID
- Yousefzadeh, Matthew J.
- Flores, Rafael R.
- Zhu, Yi
- Schmiechen, Zoe C.
- Trussoni, Christy E.
- Cui, Yuxiang
- Lee, Kyoo-A
- McGowan, Sara J.
- Burrack, Adam L.
- Wang, Dong
- Dong, Qing
- Lu, Aiping
- Sano, Tokio
- Pillai, Smitha P. S.
- Ladiges, Warren C.
- Burd, Christin E.
- Lewis, Sara E.
- LaRusso, Nicholas F.
- Vo, Nam V.
- Wang, Yinsheng
- Huard, Johnny
- Stromnes, Ingunn M.
- Robbins, Paul D.
- Niedernhofer, Laura J.
- Venue
- Nature
- Published
- 2021-05-12
- Volume
- 594
- Issue
- 7861
- Pages
- 100-105
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC8684299
- OpenAlex
- W3161778279
- Cited by
- 972
- References
- 43
- Citations by year
- 2026: 176 · 2025: 219 · 2024: 219 · 2023: 186 · 2022: 131 · 2021: 41
- FWCI
- 91.03
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institute on Aging (P01AG043376, R01AG059711, R01AG067193, R01AG044376, R56AG059676, R56AG058543, T32AG029796, U19AG056278, P01AG062413, R01AG063543)
- National Cancer Institute (R01CA249393, R01CA255039)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK084567)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- immunosenescence, cellular senescence, ERCC1, DNA repair, endogenous DNA damage, hematopoietic cells, rapamycin, senolytics, healthy aging
- MeSH terms
- Immunosenescence, Healthy Aging, Aging, Animals, DNA Damage, DNA Repair, DNA-Binding Proteins, Endonucleases, Female, Homeostasis, Immune System, Male, Organ Specificity, Rejuvenation, Spleen, Sirolimus, Mice
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