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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]
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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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“Senescent cells have a bystander effect on surrounding cells that often acquire a secondary senescence-like phenotype (Yousefzadeh et al., 2021).”
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“An aged immune system drives senescence and aging of solid organs, as can increased autoimmune susceptibility.(62) It is therefore difficult to draw a clear line between aging and lupus-like phenotypes, which have distinct characteristics but also intersect with each other.”
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“As recently released, Yamagishi et al., emphasized that Gasdermin-D-mediated pore formation significantly upregulated IL-1β and IL-33 secretion, which acts as a promotor in non-alcoholic steatohepatitis (NASH)-associated HCC progression [53,54].”
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“The floxed allele of Ercc1 was constructed by inserting the cDNA for exons 7– 10 of Ercc1 along with a neomycin cassette all flanked by loxP sites into the Ercc1 locus in intron 6 (Figure S1a) (Yousefzadeh et al., 2021).”
MethodSelf-citationBiomarkers of Aging and Relevant Evaluation Techniques: A Comprehensive Review
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“In mouse models with accelerated immune aging and natural aging, spleen B cells showed increased expression of p16 INK4a and p21 Cip1 but limited expression of SASP compared to other immune subtypes [100].”
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Self-citationThe ageing immune system as a driver of systemic ageing
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Self-citationAntiaging Vaccines Targeting Senescent Cells
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“6,7 Experiments demonstrate both cell autonomous and nonautonomous mechanisms: transplanted old or mutant splenocytes can confer aging phenotypes, whereas transplanted young normal splenocytes can suppress senescence in the mutant mice.”
Shrestha, N., Chaturvedi, P., Zhu, X., Dee, M. J., George, V., Janney, C., Egan, J. O., Liu, B., Foster, M., Marsala, L. I., et al. (2023) · Aging Cell · doi:10.1111/acel.13806 · Cited by 27
“It has been recently shown that an aged immune system drives senescence and aging of solid organs (Yousefzadeh et al., 2021).”
BackgroundThe immune landscape of murine skeletal muscle regeneration and aging
Sousa, N. S., Bica, M., Brás, M. F., Sousa, A. C., Antunes, I. B., Encarnação, I. A., Costa, T. M., Martins, I. B., Barbosa‐Morais, N. L., Sousa‐Victor, P., et al. (2024) · Cell Reports · doi:10.1016/j.celrep.2024.114975 · Cited by 30
Circulating biomarkers of inflammaging as potential predictors of COVID-19 severe outcomes
Sabbatinelli, J., Matacchione, G., Giuliani, A., Ramini, D., Rippo, M. R., Procopio, A. D., Bonafè, M., & Olivieri, F. (2022) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2022.111667 · Cited by 28
Association between Immunosenescence, Mitochondrial Dysfunction and Frailty Syndrome in Older Adults
Buondonno, I., Sassi, F., Cattaneo, F., & D’Amelio, P. (2022) · Cells · doi:10.3390/cells12010044 · Cited by 29
“Several biological mechanisms account for unhealthy aging and the development of frailty; amongst these is the deregulation of the immune system, which reduces the ability to fight against microorganisms and cancer invasion, known as “immunosenescence” [4,5].”
BackgroundShireman, J. M., Gonugunta, N., Zhao, L., Pattnaik, A., Distler, E., Her, S., Wang, X., Das, R., Galipeau, J., & Dey, M. (2023) · Aging Cell · doi:10.1111/acel.13864 · Cited by 26
“Furthermore, we and others have shown that by driving immune senescence GBM IDHwt may itself accelerate age- related immune dysfunction (Falci et al., 2013; Huff et al., 2019, 2021; Kanesvaran et al., 2018; Ladomersky et al., 2020; Yousefzadeh et al., 2021).”
BackgroundCellular Senescence, Inflammation, and Cancer in the Gastrointestinal Tract
Choi, E. L., Taheri, N., Chandra, A., & Hayashi, Y. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24129810 · Cited by 29
“In mice that were genetically modified to have an accelerated senescence of the immune system, T cell numbers were found to have significantly reduced, which led to a compromised immune response [39].”
BackgroundCounteracting Immunosenescence—Which Therapeutic Strategies Are Promising?
Hieber, C., Grabbe, S., & Bros, M. (2023) · Biomolecules · doi:10.3390/biom13071085 · Cited by 30
Immunosenescence and macrophages: From basics to therapeutics
Zhu, H., Shen, F., Liao, T., Qian, H., & Liu, Y. (2023) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2023.106479 · Cited by 30
Two types of human TCR differentially regulate reactivity to self and non-self antigens
Trofimov, A., Brouillard, P., Larouche, J., Séguin, J., Laverdure, J., Brasey, A., Ehx, G., Roy, D., Busque, L., Lachance, S., et al. (2022) · iScience · doi:10.1016/j.isci.2022.104968 · Cited by 30
“Thymic involution is instrumental in decreasing immunocompetence with age and represents a major public health issue, as illustrated by the COVID pandemic (Mittelbrunn and Kroemer, 2021; Palmer et al., 2018; Yousefzadeh et al., 2021).”
BackgroundWei, M., Zhang, G., Huang, Z., Ding, X., Sun, Q., Zhang, Y., Zhu, R., Guan, H., & Ji, M. J. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02855-1 · Cited by 26
“There is evidence that both immune aging and lowgrade chronic inflammation, as a feature of aging, are associated with impaired autophagic flux in microglia [32].”
BackgroundLu, W., Chen, X. '., & Liu, M. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1547763 · Cited by 26
Immunological biomarkers of aging
Wu, F., Mu, W., Markov, N. T., Fuentealba, M., Halaweh, H., Senchyna, F., Manwaring-Mueller, M., Winer, D. A., & Furman, D. (2025) · The Journal of Immunology · doi:10.1093/jimmun/vkae036 · Cited by 28
“175 This deficiency not only leads to senescence within the immune system, but also results in the degeneration of distant solid organs.”
Aging reshapes the adaptive immune system from healer to saboteur
Delgado-Pulido, S., Yousefzadeh, M. J., & Mittelbrunn, M. (2025) · Nature Aging · doi:10.1038/s43587-025-00906-1 · Cited by 29
“Adoptive transfer of splenocytes was capable of transiently reducing senescent cell burden and tissue dysfunction in progeroid mice 18 .”
Self-citationElastin-derived extracellular matrix fragments drive aging through innate immune activation
Yi, J., Wang, Y., Sui, H., Chen, Z., Ye, T., Zhong, Y., Qian, J., Wu, B., Huang, J., Tian, T., et al. (2025) · Nature Aging · doi:10.1038/s43587-025-00961-8 · Cited by 31
“Specific induction of aging in the entire immune system or only T cells causes systemic chronic inflammation and aging of solid organs 19,20 .”
InfluentialSelf-citationImmune dysfunction in Alzheimer disease
Butovsky, O., Rosenzweig, N., Kleemann, K. L., Jorfi, M., Kuchroo, V. K., Tanzi, R. E., & Weiner, H. L. (2025) · Nature reviews. Neuroscience · doi:10.1038/s41583-025-00997-0 · Cited by 41
“Indeed, there is evidence from studies in mice that accelerating immune ageing can hasten neurodegenerative processes, whereas counteracting immune ageing can mitigate them 30 .”
Application of mesenchymal stem cells for anti-senescence and clinical challenges
Wang, Y., Gao, T., & Wang, B. (2023) · Stem Cell Research & Therapy · doi:10.1186/s13287-023-03497-z · Cited by 27
“In addition, senescence can lead to the aging of the immune system, disrupting the homeostasis of macrophages [4] and increasing morbidity and mortality in the elderly [5].”
BackgroundSelf-citationBaghdadi, M., Nespital, T., Monzó, C., Deelen, J., Grönke, S., & Partridge, L. (2024) · Molecular Metabolism · doi:10.1016/j.molmet.2024.101902 · Cited by 28
“The ageing spleen is a major organ for driving non-cell autonomous in fl ammation in several systemic tissues [68].”
BackgroundHudson, H. R., Sun, X., & Orr, M. E. (2025) · Neurotherapeutics · doi:10.1016/j.neurot.2024.e00519 · Cited by 28
Targeting cIAP2 in a novel senolytic strategy prevents glioblastoma recurrence after radiotherapy
Tomimatsu, N., Cristofaro, L. F. M. D., Kanji, S., Samentar, L., Jordan, B. R., Kittler, R., Habib, A. A., Espíndola‐Netto, J. M., Tchkonia, T., Kirkland, J. L., et al. (2025) · EMBO Molecular Medicine · doi:10.1038/s44321-025-00201-x · Cited by 32
“Such spreading of the SASP from senescent to naive cells is very similar to “ senescence spreading ” from damaged to undamaged cells that has been previously reported (Acosta et al, 2013; Nelson et al, 2012; Vicente et al, 2016; Xu et al, 2018; Yousefzadeh et al, 2021).”
The secretome of senescent monocytes predicts age-related clinical outcomes in humans
Olinger, B., Banarjee, R., Dey, A. K., Tsitsipatis, D., Tanaka, T., Ram, A., Nyunt, T., Daya, G. N., Peng, Z., Shrivastava, M., et al. (2025) · Nature Aging · doi:10.1038/s43587-025-00877-3 · Cited by 32
Aging microenvironment in osteoarthritis focusing on early-stage alterations and targeted therapies
Dang, Y., Liu, Y., Zhang, B., & Zhang, X. (2025) · Bone Research · doi:10.1038/s41413-025-00465-6 · Cited by 30
“11,12 Thus, senescence likely affects various cell types in the OA microenvironment beyond chondrocytes.”
Senescent Stromal Cells in the Tumor Microenvironment: Victims or Accomplices?
Ye, M., Huang, X., Wu, Q., & Liu, F. (2023) · Cancers · doi:10.3390/cancers15071927 · Cited by 27
“This speculation is yet to be proven and is mainly based on findings from recent studies that elucidate the engagement of senescent immune cells in the process of solid tissue senescence [74,75].”
BackgroundTelomerase reverse transcriptase and neurodegenerative diseases
Yu, X., Liu, M., Zheng, C., Liu, Y., Wang, Z., & Wang, Z.-Y. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1165632 · Cited by 25
“A recent study found that T cells play an important role in the brain and considering the relationship between aging and neurodegenerative diseases (51), it is not difficult to imagine that a deeper study of T cells may provide important therapeutic clues for aging-related diseases, including neurodegenerative disease…”
BackgroundGenetic and clinical determinants of telomere length
Allaire, P., He, J., Mayer, J. E., Moat, L. F., Gerstenberger, P., Wilhorn, R., Strutz, S., Kim, D. S. L., Zeng, C., Cox, N. J., et al. (2023) · Human Genetics and Genomics Advances · doi:10.1016/j.xhgg.2023.100201 · Cited by 24
“Accumulation of senescence cells in organs over time is one of the driving causes of chronic organ inflammation, organ failure, and diseases of advanced age.(4,5)”
BackgroundLessons of Vascular Specialization From Secondary Lymphoid Organ Lymphatic Endothelial Cells
Arroz‐Madeira, S., Bekkhus, T., Ulvmar, M. H., & Petrova, T. V. (2023) · Circulation Research · doi:10.1161/circresaha.123.322136 · Cited by 27
Impact of senolytic treatment on immunity, aging, and disease
Lorenzo, E. C., Torrance, B. L., & Haynes, L. (2023) · Frontiers in Aging · doi:10.3389/fragi.2023.1161799 · Cited by 28
B Cells Dynamic in Aging and the Implications of Nutritional Regulation
Yu, Y., Lu, C., Yu, W., Lei, Y., Sun, S., Liu, P., Bai, F., Chen, Y., & Chen, J. (2024) · Nutrients · doi:10.3390/nu16040487 · Cited by 29
Shi, J., Lai, Z., Zhou, W., Yang, H., Zhang, T., Sun, J., Zhao, J., & Li, M. (2024) · The EMBO Journal · doi:10.1038/s44318-024-00220-3 · Cited by 27
“Metformin, resveratrol, and rapamycin are reported as anti-aging drug candidates that delay or improve the aging process (Chen et al, 2022; Grinan-Ferre et al, 2021; Kulkarni et al, 2020; Yousefzadeh et al, 2021).”
Genetic origins, regulators, and biomarkers of cellular senescence
Torres, G., Salladay-Perez, I. A., Dhingra, A., & Covarrubias, A. J. (2024) · Trends in Genetics · doi:10.1016/j.tig.2024.08.007 · Cited by 24
Targeting immunosenescence for improved tumor immunotherapy
Liu, Z., Zuo, L., Zhou, Z., Liu, S., Ba, Y., Zuo, A., Ren, Y., Zhang, C., Chen, Y., Ma, H., et al. (2024) · MedComm · doi:10.1002/mco2.777 · Cited by 24
“253 What’s more, SIRP α DCs have been revealed to regulate homeostasis of fibroblastic reticular cells via TNF receptor ligands in white pulp of adult spleen.”
BackgroundRemodeling of tumor microenvironment by cellular senescence and immunosenescence in cervical cancer
He, Y., Qiu, Y., Yang, X., Lu, G., & Zhao, S. (2024) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2024.11.002 · Cited by 25
Prummel, K. D., Woods, K., Kholmatov, M. M., Schmitt, E. C., Vlachou, E. P., Labyadh, M., Wehner, R., Poschmann, G., Stühler, K., Winter, S., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-65803-y · Cited by 30
The tumor suppression theory of aging
Wolf, A. M. (2021) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2021.111583 · Cited by 27
Ke, J., Yu, J.-Y., Gao, B., Hu, F., Xu, F., Yao, G., & Bao, G. (2022) · Food & Function · doi:10.1039/d2fo01795d · Cited by 26
Nutrition and immunity: perspectives on key issues and next steps
Dunbar, C. L., Aukema, H. M., Calder, P. C., Gibson, D. L., Henrickson, S. E., Khan, S., Mailhot, G., Panahi, S., Tabung, F. K., Tom, M., et al. (2023) · Applied Physiology, Nutrition, and Metabolism · doi:10.1139/apnm-2022-0276 · Cited by 24
Chen, H., Wang, Q., Li, J., Li, Y., Chen, A., Zhou, J., Zhao, J., Mao, Z., Zhou, Z., Zhang, J., et al. (2023) · Aging and Disease · doi:10.14336/ad.2023.0320 · Cited by 24
“According to a previous study, splenocyte transplantation from aged mice induces the senescence of multiple organs [52].”
BackgroundSelf-citationWu, Y., Hu, S. S., Zhang, R., Goplen, N. P., Gao, X., Narasimhan, H., Shi, A., Chen, Y. M., Li, Y., Zang, C., et al. (2023) · iScience · doi:10.1016/j.isci.2023.107197 · Cited by 25
“However, senescence in immune cells may also be important for the aging of lung.(19) For instance, adoptive transfer of the splenocytes from aged, but not young mice could induce enhanced senescence in the lung of recipient mice,(19) suggesting a prominent role for aged immune cells in shaping the aged lung environmen…”
BackgroundInfluentialTranslational Frontiers and Clinical Opportunities of Immunologically Fitted Radiotherapy
Morel, D., Robert, C., Nikos Paragios, A., Grégoire, V., & Deutsch, É. (2024) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-23-3632 · Cited by 29
“Surviving lymphocytes exposed to radiation displayed signi fi cantly activated DNA damage response pathways (68), the high burden of endogenous DNA damage being a direct contributor to senescence induction (73).”
BackgroundUnraveling anti-aging mystery of green tea in C. elegans: Chemical truth and multiple mechanisms
Ke, J., Li, J.-Y., Yang, Z. M., Wu, H.-Y., Yu, J.-Y., Yang, Y., Chen, C., Zhou, P., Hua, F., Wang, W., et al. (2024) · Food Chemistry · doi:10.1016/j.foodchem.2024.140510 · Cited by 26
The role of macrophage plasticity in neurodegenerative diseases
Ma, H., Zhu, M., Chen, M., Li, X., & Feng, X. (2024) · Biomarker Research · doi:10.1186/s40364-024-00624-7 · Cited by 24
“Moreover, transplantation of splenocytes from young mice has been shown to delay the aging process in senescent mice [144], suggesting that the spleen is a potential therapeutic target for AD.”
BackgroundSenescent neutrophils: a hidden role in cancer progression
Rys, R. N., & Calcinotto, A. (2024) · Trends in Cell Biology · doi:10.1016/j.tcb.2024.09.001 · Cited by 26
How age affects human hematopoietic stem and progenitor cells and the strategies to mitigate aging
Li, X., Wang, J., Hu, L., & Cheng, T. (2025) · Experimental Hematology · doi:10.1016/j.exphem.2025.104711 · Cited by 25
Beyond the Hayflick limit: How microbes influence cellular aging
Abavisani, M., Faraji, S., Ebadpour, N., Karav, S., & Sahebkar, A. (2025) · Ageing Research Reviews · doi:10.1016/j.arr.2025.102657 · Cited by 24
Wang, L., Jiang, W., Yang, M., Danzeng, Q., Liu, S., & Cui, M. (2025) · Cell Communication and Signaling · doi:10.1186/s12964-025-02275-z · Cited by 28
“Immunosenescence, particularly excessive T cell senescence, ultimately results in a deterioration in immune system function and induces potential tumorigenic process [11].”
The potential of Senolytics in transplantation
Matsunaga, T., Iske, J., Schroeter, A., Azuma, H., Zhou, H., & Tullius, S. G. (2021) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2021.111582 · Cited by 22
Senescence and Type 2 Diabetic Cardiomyopathy: How Young Can You Die of Old Age?
Henson, S. M., & Aksentijević, D. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.716517 · Cited by 23
“They were able to demonstrate that solid organs also showed increased senescence and damage, indicating that senescent, aged immune cells can promote systemic ageing (Yousefzadeh et al., 2021).”
BackgroundAging Leukocytes and the Inflammatory Microenvironment of the Adipose Tissue
Dahlquist, K. J. V., & Camell, C. D. (2021) · Diabetes · doi:10.2337/dbi21-0013 · Cited by 25
Mechanisms of Post-critical Illness Cardiovascular Disease
Owen, A., Patel, J. M., Parekh, D., & Bangash, M. N. (2022) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2022.854421 · Cited by 22
“Furthermore, findings that immunosenescence alone can drive tissue aging (217), and that biological age can be accurately predicted by both cardiovascular biomarker scores and an associated immune-aging score based on various markers of immunosenescence, such as T-cell PD-1 receptor positivity, lends further support t…”
BackgroundAnthracycline-induced cardiotoxicity and senescence
Booth, L. K., Redgrave, R. E., Folaranmi, O., Gill, J. H., & Richardson, G. D. (2022) · Frontiers in Aging · doi:10.3389/fragi.2022.1058435 · Cited by 25
“, 2016) and are the mainstay class of chemotherapeutics against a diverse range of malignancies (Yousefzadeh et al., 2021).”
Background
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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