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Senolytic CAR T cells reverse senescence-associated pathologies
Open accessAbstract
Cellular senescence is characterized by stable cell-cycle arrest and a secretory program that modulates the tissue microenvironment1,2. Physiologically, senescence serves as a tumour-suppressive mechanism that prevents the expansion of premalignant cells3,4 and has a beneficial role in wound-healing responses5,6. Pathologically, the aberrant accumulation of senescent cells generates an inflammatory milieu that leads to chronic tissue damage and contributes to diseases such as liver and lung fibrosis, atherosclerosis, diabetes and osteoarthritis1,7. Accordingly, eliminating senescent cells from damaged tissues in mice ameliorates the symptoms of these pathologies and even promotes longevity1,2,8–10. Here we test the therapeutic concept that chimeric antigen receptor (CAR) T cells that target senescent cells can be effective senolytic agents. We identify the urokinase-type plasminogen activator receptor (uPAR)11 as a cell-surface protein that is broadly induced during senescence and show that uPAR-specific CAR T cells efficiently ablate senescent cells in vitro and in vivo. CAR T cells that target uPAR extend the survival of mice with lung adenocarcinoma that are treated with a senescence-inducing combination of drugs, and restore tissue homeostasis in mice in which liver fibrosis is induced chemically or by diet. These results establish the therapeutic potential of senolytic CAR T cells for senescence-associated diseases. Chimeric antigen receptor (CAR) T cells targeting uPAR, a cell-surface protein that is upregulated on senescent cells, eliminate senescent cells in vitro and in vivo and reduce liver fibrosis in mice.
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“Certain cell surface proteins tend to be more highly expressed by senescent cells than most other cell types, which prompted development of engineered chimeric antigen receptor (CAR) T cells, vaccines and antibody–drug conjugates targeting these cell surface markers.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [96]
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
“Each of these approaches eliminates senescent cells, although in some cases, activated macrophages and other non-senescent cell types are also affected96–99.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [96]
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
“It was found that anti-uPAR-CAR-T cells were effective in removing senescent cells in vitro and pre-cancerous and malignant cells in mouse models of liver and lung in the presence of potentially toxic.350”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [350]
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
“Mice with lung adenocarcinomas were first exposed to a combination of MEK and CDK4/6 inhibitors to induce senescence, and then received uPAR- targeting CAR Tcells to selectively kill those senescent cells, leading to a marked delay in tumour growth 22 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [22]
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
“Genome-wide CRISPR screens and transcriptomic profiling have identified several promising SnC-specific targets, with urokinase-type plasminogen activator receptor (uPAR) emerging as a leading candidate63,64”
From Emerging strategies in senotherapeutics: from broad-spectrum senolysis to precision reprogramming (2026) · cites this paper as [63]
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“Exciting recent work has demonstrated that senolytic CAR T cell therapy can attenuate senescence-associated diseases226.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [226]
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In the citing paper
“and PLAUR (uPAR) is associated with extracellular remodeling and increased secretion by senescent cells (Amor et al, 2020).”
From Distinct senotypes in p16- and p21-positive cells across human and mouse aging tissues (2025) · cites this paper as Amor et al, 2020
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“Amor et al. (2020) engineered chimeric antigen receptor (CAR) T cells recognizing uPAR, a protein expressed by senescent cells, a strategy that mirrors normal senescence immunosurveillance.”
From Senescence and the SASP: many therapeutic avenues (2020) · cites this paper as Amor et al. 2020
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In the citing paper
“these “senolytic CAR T cells” can be used not just as an anticancer therapy, but to treat other senescence-associated disorders, such as nonalcoholic steatohepatitis (NASH) (Amor et al. 2020).”
From Senescence and the SASP: many therapeutic avenues (2020) · cites this paper as Amor et al. 2020
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In the citing paper
“Other plasma membrane proteins whose expression has also been reported to change during senescence are receptor- type tyrosine protein phosphatase DEP-1, β 2 -microglobulin, membrane- bound oxidized vimentin, dipeptidyl peptidase 4 and urokinase- type plasminogen activator receptor (uPAR) 22,61,62 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [22]
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In the citing paper
“Moreover, CAR Tcells targeting uPAR on the surface of senescent cells have been developed as promising cell- based senolytics 22 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [22]
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In the citing paper
“chimeric antigen receptor redirected T (CAR-T) cells that target the senescent cell-specific surface molecule uPA receptor [116]”
From The role of cellular senescence and SASP in tumour microenvironment (2023) · cites this paper as [116]
The cited source says what the claim attributes to it.
In the citing paper
“In particular, antibodies directed against the glycoprotein NMB (GPNMB) 202 and CAR T cells directed against the receptor uPAR 203 attenuate senescence-associated disease models in mice.”
From Hallmarks of aging: An expanding universe (2023) · cites this paper as [203]
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In the citing paper
“Additionally, CXCL16 is upregulated in aging and inflammatory conditions linked to senescence”
From Distinct senotypes in p16- and p21-positive cells across human and mouse aging tissues (2025) · cites this paper as Amor et al, 2020
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
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“transplantation of a small proportion of senescent cells or injection of chimeric antigen receptor (CAR) Tcells with a senescent phenotype accelerated physical dysfunction and reduced lifespan 21,22”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [22]
Experimental — accuracy not yet measuredIn the citing paper
“This approach was successfully validated by a study that used CAR-T to deplete only HSCs that expressed the senescence marker urokinase plasminogen activator receptor (uPAR), thereby improving inflammation and fibrosis (128).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [128]
In the citing paper
“In mouse models, CAR T cells directed against uPAR (urokinase-type plasminogen activator receptor), which is abundantly present on senescent cells, ameliorates experimental liver fibrosis.146”
From An integrated view of anti-inflammatory and antifibrotic targets for the treatment of NASH (2023) · cites this paper as [146]
In the citing paper
“Moreover, recent studies have shown that uPAR-specific CAR-T cells can effectively eliminate senescent cells in vitro and in vivo and prolong the survival of lung adenocarcinoma mice [127].”
From Immunosenescence: a key player in cancer development (2020) · cites this paper as [127]
In the citing paper
“Studies have begun to reveal the remarkable heterogeneity of cellular senescence in different tissues, highlighting the importance of cellular senescence markers beyond p16 – including Cdkn1a (p21) [7–10], Cdkn2d (p19) [11], uPAR [12], and glycoprotein non-metastatic melanoma protein B (GPNMB) [13] – and emphasizing the urgent need for a better understanding of senescent cell heterogeneity.”
From The heterogeneity of cellular senescence: insights at the single-cell level (2023) · cites this paper as [12]
In the citing paper
“In another study, urokinase plasminogen activator receptor (uPAR), was identified as a unique senescence marker by comparing differentially expressed genes in bulk RNA-seq datasets of three known mouse models of senescence, and was validated by flow cytometry [12].”
From The heterogeneity of cellular senescence: insights at the single-cell level (2023) · cites this paper as [12]
In the citing paper
“Elimination of uPAR-expressing cells with chimeric antigen receptor (CAR) T cells specifically kills senescent cells both in vivo and in vitro, and extends the lifespan of mice with lung adenocarcinoma [12].”
From The heterogeneity of cellular senescence: insights at the single-cell level (2023) · cites this paper as [12]
In the citing paper
“Similarly, chimeric antigen receptor (CAR) T cells targeting the urokinase-type plasminogen activator receptor (uPAR), reported to be a specific cell surface marker in certain senescent cell populations, effectively ablated senescent cells in vitro and in murine models of lung adenocarcinomas and liver fibrosis (49).”
From Exercise Counters the Age-Related Accumulation of Senescent Cells (2022) · cites this paper as [49]
In the citing paper
“The success of immunotherapies in different forms of cancer have also led to proof-of-concept studies for targeting senescent cells (Amor et al., 2020; Kim et al., 2017).”
From Skeletal muscle aging, cellular senescence, and senotherapeutics: current knowledge and future directions (2021) · cites this paper as Amor et al., 2020
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Self-citation
Metadata
- Authors
- Amor, C., Feucht, J., Leibold, J., Ho, Y.-J., Zhu, C., Alonso-Curbelo, D., Mansilla-Soto, J., Boyer, J. A., Li, X., Giavridis, T., Kulick, A., Houlihan, S., Peerschke, E., Friedman, S. L., Ponomarev, V., Piersigilli, A., Sadelain, M., & Lowe, S. W.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Sadelain, Michel
- Lowe, Scott W.
- ORCID
- Venue
- Nature
- Published
- 2020-06-17
- Volume
- 583
- Issue
- 7814
- Pages
- 127-132
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC7583560
- OpenAlex
- W3036603151
- Semantic Scholar
- 04e18a651e78de49d44a74b1db3d968208b4c3a1
- Cited by
- 1,098
- References
- 60
- Citations by year
- 2026: 194 · 2025: 236 · 2024: 208 · 2023: 147 · 2022: 135 · 2021: 131 · 2020: 45
- FWCI
- 68.89
- Type
- journal article
- Language
- en
- Update notices
- correction (2024-02-21)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institutes of Health (U54OD020355)
- National Institute on Aging (AG065396, R56AG016379, R01AG016379, R01AG065396)
- National Cancer Institute (P01CA129243, P30CA008748)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK056621)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › CAR-T cell therapy research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- cellular senescence, chimeric antigen receptor T cells, urokinase-type plasminogen activator receptor, liver fibrosis, lung adenocarcinoma, senescence-associated secretory phenotype, tissue homeostasis
- MeSH terms
- Receptors, Chimeric Antigen, Adenocarcinoma, Aging, Animals, Carbon Tetrachloride, Female, Humans, Liver Cirrhosis, Longevity, Lung Neoplasms, Male, Receptors, Cell Surface, Rejuvenation, T-Lymphocytes, T-Lymphocytes, Cytotoxic, Cellular Senescence, Mice, Receptors, Urokinase Plasminogen Activator, Heterografts
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