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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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In the citing paper
“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]
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.
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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Meeting Report: Aging Research and Drug Discovery
Meron, E., Thaysen, M., Angeli, S., Antebi, A., Barzilai, N., Baur, J. A., Bekker‐Jensen, S., Birkisdóttir, M. B., Bischof, E. Y., Bruening, J., et al. (2022) · Aging · doi:10.18632/aging.203859 · Cited by 7
“She further showed that senescent cells in old mice cause an over-reaction to PAMPs, driving a cytokine storm that drives organ failure and death upon infection with a pathogen such as β-coronaviruses, an effect that can be ameliorated by treatment with the senolytic fisetin [35, 36].”
BackgroundSelf-citationPredictors of Toxicity Among Older Adults with Cancer.
Extermann, M., Chetty, I., Brown, S., Al-Jumayli, M., & Movsas, B. (2022) · Seminars in Radiation Oncology · doi:10.1016/j.semradonc.2021.11.004 · Cited by 3
Lessons from Sicilian centenarians for anti-ageing medicine. The Oxi-inflammatory status
Caruso, C., Accardi, G., Aiello, A., Calabrò, A., Ligotti, M. E., & Candore, G. (2022) · Translational Medicine UniSa · doi:10.37825/2239-9747.1036 · Cited by 5
Single cell decomposition of multicellular aging programs associated with impaired lung regenerationPreprint
Gote-Schniering, J., Melo-Narváez, M. C., Boosarpu, G., Lauer, D., Prakki, S. R. S., Wang, H., Brunner, M., Khan, S., Ansari, M., Ammeter, M., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.07.24.666371 · Cited by 7
“It is possible that mechanisms of immune-mediated impairment of stem cell niches, as shown here for the lung, may act in a similar way across organ systems 7,47 .”
Senescence as a therapeutic target
Meyer, K. R., Lopez-Dominguez, J. A., Maus, M., Kovatcheva, M., & Serrano, M. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-822514-1.00014-6 · Cited by 5
Chen, K., Ling, J., Zhou, X., Zhang, M., Long, Q., & Huang, L. (2024) · Journal of Holistic Integrative Pharmacy · doi:10.1016/j.jhip.2024.05.001 · Cited by 5
The potential of flavonoids to mitigate cellular senescence in cardiovascular disease
Zheng, H., Li, T., Hu, Z., Zheng, Q., & Wang, J. (2024) · Biogerontology · doi:10.1007/s10522-024-10141-7 · Cited by 6
“Intensive mechanism studies have shown that a variety of factors can induce cellular senescence, such as telomeres shortening, DNA damage and reactive oxygen species (ROS) (Davalli et al. 2016; Dungan et al. 2022; Yousefzadeh et al. 2021).”
Ma, K., Niu, J., Zeng, L., Tian, J., & Zhang, Y. (2025) · Neurochemical Research · doi:10.1007/s11064-025-04373-3 · Cited by 6
“Immunosenescence and chronic inflammation are the most obvious features of aging [1 ].”
Stefens, S. J. M., van der Linden, J., Heredia‐Genestar, J. M., Brandt, R. M. C., Barnhoorn, S., Nieuwenhuizen‐Bakker, I., van Vliet, N., Odijk, J. H. M., Ridwan, Y. R., Stuijts, D., et al. (2025) · Aging Cell · doi:10.1111/acel.70062 · Cited by 6
Gong, Y., Wang, Y., Delgado‐Peraza, F., Nogueras‐Ortiz, C. J., Hooten, N. N., Croteau, D. L., Temre, M. K., Molnar, A. E., Bodogai, M., Zou, A., et al. (2025) · iScience · doi:10.1016/j.isci.2025.112661 · Cited by 5
“29 This finding suggests that a mechanism via altered intercellular communication may contribute to systemic aging.”
Self-citationResearch progress on blood therapy for anti-aging
Liu, S., Wang, S., Dong, Y., Yang, S., & Yao, C. (2025) · Journal of Advanced Research · doi:10.1016/j.jare.2025.07.039 · Cited by 5
“Given that acute immunosenes-cence accelerates human aging and mortality [ 249,250], we pro-pose an innovative therapeutic strategy comprising two phases: Firstly, removal of pro-aging factors.”
Seshadri, V., Chng, C., Tyler, J., Adikerta, C., Baghaei, K., Wang, Y., Gueven, N., Ricardo, S. D., & Azimi, I. (2025) · Aging Cell · doi:10.1111/acel.70209 · Cited by 7
Self-citationDeng, Y., He, X., Peng, J., Pan, Y., Luo, Y., Ruan, Y., Hou, J., Jiang, B., Li, X., Liang, X., et al. (2025) · Cell Death and Disease · doi:10.1038/s41419-025-08007-y · Cited by 8
Yin, H., Zhou, S., Shen, K., Chen, H., Yang, M., Deng, Y., Chang, C., & Wu, H. (2025) · Clinical Reviews in Allergy & Immunology · doi:10.1007/s12016-025-09109-3 · Cited by 6
“…decarboxylase (ACMSD) to boost endogenous NAD ⁺ synthesis further validates this strategy [113]. mTOR inhibition by rapamycin suppresses glycolysis and reduces senescence markers (p16/p21) and SASP factors (MCP-1/TNF) in immunosenescent models, restoring T cell functionality [114, 115].”
Adiponectin and aging: Mechanistic insights, clinical paradox, and therapeutic horizons
McGregor, E. R., Osterbauer, K. J., Gustafson, G. E., Clark, J. P., Rhoads, T. W., & Anderson, R. M. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103059 · Cited by 6
“…production of ATP (Amorim et al., 2022; Harrington et al., 2023; Granath-Panelo and Kajimura, 2024; Monzel et al., 2023); cell fate determinants including p53/p44 (Vaddavalli and Schumacher, 2022; Huang et al., 2024), and cellular senescence (Di Micco et al., 2021; Yousefzadeh et al., 2021).”
Neurosenescence, inflammaging and neuroinflammation in neurodegenerative disorders
Kempuraj, D., Babu, P. R. R., Jayakumar, N., Belur, M. G., Cohan, C. H., Sharma, A., Sanchez-Guerrero, E., Anderson, T., Kong, D., Chinnappan, B., et al. (2026) · Frontiers in Aging · doi:10.3389/fragi.2026.1756670 · Cited by 6
“Increased senescence and damage in non-lymphoid organs indicate that senescent and aged immune cells can contribute to systemic aging, representing an important therapeutic target to extend healthy ageing (Yousefzadeh et al., 2021).”
CD4 CTLs in supercentenarians: Signs of adaptive expansion in healthy aging
Hashimoto, K., Kojima-Ishiyama, M., Inokuchi, H., Tagami, M., Sasaki, T., Mizuguchi, K., Okazaki, Y., Taniuchi, I., Ishigaki, K., Hirose, N., et al. (2026) · Cell Reports · doi:10.1016/j.celrep.2026.117728 · Cited by 5
Cox, L. S. (2022) · The Journal of the Economics of Ageing · doi:10.1016/j.jeoa.2022.100423 · Cited by 6
Reconstructing the immunosenescence core pathway reveals global characteristics in pan-cancer
Zhang, Y., Sun, Y., Gan, J., Zhou, H., Guo, S., Wang, X., Zheng, W., Zheng, W., Zhao, X., Zhang, Y., et al. (2023) · Cancer Immunology Immunotherapy · doi:10.1007/s00262-023-03521-4 · Cited by 5
“We found that OSI-027 (A7486), Rapamycin, PRIMA-1MET (APR-246), Venetoclax, and MIRA-1 showed robust antitumor activity in HNSC. Studies have shown that Rapamycin treatment in mice can reduce immune cell senescence markers and improve immune function [33].”
BackgroundCho, H.-M., Choe, S.-H., Lee, J.-R., Park, H., Ko, M.-G., Lee, Y.-J., Lee, H.-Y., Park, S. H., Park, S.-J., Kim, Y., et al. (2024) · npj Aging · doi:10.1038/s41514-024-00158-0 · Cited by 5
Terminally differentiated effector memory T cells in kidney transplant recipients: New crossroads
Laecke, S. V., & Glorieux, G. (2024) · American Journal of Transplantation · doi:10.1016/j.ajt.2024.10.001 · Cited by 5
Cellular senescence as a source of chronic microinflammation that promotes the aging process
Nakanishi, M. (2025) · Proceedings of the Japan Academy Series B · doi:10.2183/pjab.101.014 · Cited by 5
Yang, C., Xu, Y. J., Gong, F., Li, S., Huang, Z., Huang, Z., Wang, M., Li, H., & Huang, H. (2025) · Frontiers in Pharmacology · doi:10.3389/fphar.2025.1565451 · Cited by 5
“It has been demonstrated that senescent immune cells play a pivotal role in the process of systemic ageing, particularly with regard to the acceleration of solid organ ageing (Yousefzadeh et al., 2021).”
Lanz, P., Wieczorek, M., Sadlon, A., Molino, C. D. G. R. C., Abderhalden, L. A., Schaer, D. J., Spahn, D. R., Freystaetter, G., Orav, E. J., Egli, A., et al. (2022) · The journal of nutrition health & aging · doi:10.1007/s12603-022-1836-2 · Cited by 5
“As people live longer, they are at an increased risk for infections due to chronic health conditions and the aging of the immune system, so called immunosenescence (11).”
Entwistle, A., Walker, S., Knecht, A. K., Strum, S. L., Shah, A. A., Podgoreanu, M. V., Pustavoitau, A., Mitin, N., & Williams, J. B. (2024) · Cardiology and Cardiovascular Medicine · doi:10.26502/fccm.92920387 · Cited by 5
Meng, Z., Lu, C., Li, J., Liao, J., Wen, H., Li, Y., Huang, F., & Zeng, Z. (2024) · Scientific Reports · doi:10.1038/s41598-024-72979-8 · Cited by 6
“Immune cells have a positive effect on senescent cells, and recent research has shown that transplanting young immune cells into aging mice could reverse the aging process 32 .”
Rob, F. I., Stebbins, R. C., Momkus, J., Martin, C. L., Harris, K. M., & Aiello, A. E. (2025) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2025.100993 · Cited by 5
Immuno(T)herapy for age‐related diseases
Gabandé‐Rodríguez, E., Pfeiffer, M., & Mittelbrunn, M. (2022) · EMBO Molecular Medicine · doi:10.15252/emmm.202216301 · Cited by 5
“…of chronic inflammation in the development of age-associated diseases has been widely accepted, a causal contribution of immune cell dysfunction to inflammaging, systemic senescence, and aging has only recently been established (Desd (cid:1) ın-Mic (cid:1) o et al , 2020; Yousefzadeh et al , 2021).”
Dietary restriction in senolysis and prevention and treatment of disease
Aminzadeh-Gohari, S., Kofler, B., & Herzog, C. M. S. (2022) · Critical Reviews in Food Science and Nutrition · doi:10.1080/10408398.2022.2153355 · Cited by 5
“…as age-related dysfunction of cell-mediated clearance, mitochondrial signaling, epigenome and chromatin organization, cytokines and chemokines, (Yousefzadeh et al. 2021; Ovadya et al. 2018), or exogenous triggers such as obesity (Wang et al. 2009; Shirakawa et al. 2016; Palmer et al. 2019) and…”
Hautalterung – zelluläre Seneszenz
Scharffetter‐Kochanek, K., Wang, Y., Makrantonaki, E., Crișan, D., Wlaschek, M., Geiger, H., & Maity, P. (2023) · Die Dermatologie · doi:10.1007/s00105-023-05201-x · Cited by 5
Self-citationGene expression in mice with endothelium-specific telomerase knockout
Gao, Z., Yu, Y., Dai, Y., Zhao, Z., Eckel‐Mahan, K. L., & Kolonin, M. G. (2023) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2023.1295072 · Cited by 5
Zhou, Z., Wei, J., & Jiang, W. (2022) · Scientific Reports · doi:10.1038/s41598-022-09549-3 · Cited by 5
Does immunosenescence drive organismal ageing via inflammageing?
Pawelec, G. (2021) · Immunity & Ageing · doi:10.1186/s12979-021-00242-z · Cited by 5
“Reciprocally, transfer of splenocytes from either younger Ercc1-deficient animals or unmanipulated old animals induced senescence in several tissues of young mice [2].”
Backgroundp16-dependent upregulation of PD-L1 impairs immunosurveillance of senescent cellsPreprint
Majewska, J., Agrawal, A., Mayo, A., Roitman, L., Chatterjee, R., Kralova, J. S., Landsberger, T., Katzenelenbogen, Y., Meir-Salame, T., Hagai, E., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.01.30.524522 · Cited by 5
“Lines of evidence suggest that the age-dependent decline of immune-mediated clearance of senescent cells depends on senescent cell-autonomous mechanisms that inhibit their removal (5, 6), and functional impairment of the aged immune system (immunosenescence) (7, 8).”
BackgroundMethodγδ T Cells Target and Ablate Senescent Cells in Aging and Alleviate Pulmonary FibrosisPreprint
Meca-Laguna, G., Admasu, T. D., Shankar, A., Barkovskaya, A., Collibee, I., Krakauer, A. A., Tran, T., Rae, M. J., & Sharma, A. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.05.05.652251 · Cited by 5
Age-associated defect in ADCC response to COVID-19 vaccine
Sievers, B. L., Altaf, M., Cheng, M. T. K., Kamelian, K., Cormie, C., Bradley, J. R., Baker, S., Graves, B., Stark, H., Hein, S., et al. (2025) · npj Vaccines · doi:10.1038/s41541-025-01196-9 · Cited by 4
Lessons in longevity from blood stem cells under protein stress
Catic, A. (2025) · Trends in Cell Biology · doi:10.1016/j.tcb.2025.06.006 · Cited by 5
“Both cellular and soluble blood components have been shown to influence organismal aging and tissue rejuvenation, though some findings remain controversial [24,25,84,85,133].”
de Mendonça, L. B., Lenz, G., & Filippi‐Chiela, E. C. (2025) · Biochemical Society Transactions · doi:10.1042/bst20253054 · Cited by 5
Boroumand, M., Dey, A. K., Cupp‐Sutton, K. A., Pierce, T., Tsitsipatis, D., Herman, A. B., Wu, S., & Basisty, N. (2025) · Analytical Chemistry · doi:10.1021/acs.analchem.5c02694 · Cited by 5
Wu, Z., Wang, C., Wang, T., Chen, J., Liang, Y., Zhou, Y., Li, C., & Zhang, S. (2025) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2025.149363 · Cited by 4
Liu, J., Li, Z., Qiong, K., Liu, Q., Sun, Y., Yan, R., Ye, H., Zhang, Y., Ren, J., Chen, H., et al. (2026) · Cellular and Molecular Immunology · doi:10.1038/s41423-025-01381-9 · Cited by 4
“However, the ef fi cacy and effectiveness of vaccination are notably diminished in older adults [6, 7], which is linked to age-related immunode fi ciency characterized by a gradual deterioration in immune function [8].”
Self-citationZhou, Z., Li, X., Wang, Y., Liang, L., Wang, C., Sun, Y., Wu, D., & Qiu, Y. (2026) · Nature Communications · doi:10.1038/s41467-026-69996-8 · Cited by 4
“Sample size was chosen based on previous experiments or based on pilot experiments to ensure the possibility of statistical analysis and to minimize the use of experimental animals based on the 3 R principles 4,13 .”
Self-citationXing, Y., Zhao, X., Li, X., Zheng, J., & Huang, W. (2026) · Biology · doi:10.3390/biology15050441 · Cited by 5
“On the other hand, profound shifts occur in intestinal immune cell populations with a reduction in naive responder cells and an increase in the proportion of senescent and memory cells [46,47].”
S100A8/A9 as a central hub in inflammaging: Cross-system mechanisms
Wang, S., Ni, Y., Feng, J., Zhang, W., Zhou, M., & Zhao, C. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103108 · Cited by 5
Wang, M., Han, Y., Yao, X., Duan, X., Wan, J., Lou, X., Yan, Y., Zheng, P., Wang, F., Zhu, L., et al. (2024) · MedComm · doi:10.1002/mco2.605 · Cited by 5
“39 Our research indicates a positive correlation between TNFR2 expression and the expression of senescence mark-WANG ers, specifically p16 Ink4a and p21 CIP .”
BackgroundWang, Y., Su, J., Su, G., Zhuangwei, N., Yiqing, Z., Suhong, C., & Lv, G. (2025) · Frontiers in Pharmacology · doi:10.3389/fphar.2025.1550357 · Cited by 4
“Aging leads to immunosenescence, causing immune function alterations such as de fi ciency, autoimmunity, and in fl ammation imbalance (Matthew et al., 2021).”
Self-citation
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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