Expression of p16 INK4a in peripheral blood T‐cells is a biomarker of human aging
Open accessAbstract
Summary: Expression of the p16 INK4a tumor suppressor sharply increases with age in most mammalian tissues, and contributes to an age‐induced functional decline of certain self‐renewing compartments. These observations have suggested that p16 INK4a expression could be a biomarker of mammalian aging. To translate this notion to human use, we determined p16 INK4a expression in cellular fractions of human whole blood, and found highest expression in peripheral blood T‐lymphocytes (PBTL). We then measured INK4/ARF transcript expression in PBTL from two independent cohorts of healthy humans (170 donors total), and analyzed their relationship with donor characteristics. Expression of p16 INK4a , but not other INK4/ARF transcripts, appeared to exponentially increase with donor chronologic age. Importantly, p16 INK4a expression did not independently correlate with gender or body‐mass index, but was significantly associated with tobacco use and physical inactivity. In addition, p16 INK4a expression was associated with plasma interleukin‐6 concentration, a marker of human frailty. These data suggest that p16 INK4a expression in PBTL is an easily measured, peripheral blood biomarker of molecular age.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Elimination of senescent cells alleviates age-related pathologies in BubR1 and Ercc1 mutant mice, but does not restore their lifespan to that of wild-type animals.
“For example, while the elimination of senescent cells alleviates age-related pathologies in BubR1 and Ercc1 mutant mice, it does not restore their lifespan to that of wild-type animals86,102.”
From Guidelines for minimal information on cellular senescence experimentation in vivo (2024) · cites this paper as [102]
The Introduction (page unavailable) reports that inactivating p16 partially rescues several age-related phenotypes in a progeroid mouse strain. It does not say that senescent cells were eliminated, address Ercc1 mutant mice, or compare the mutants’ lifespan with that of wild-type animals. (LLM, conf=0.83)
Experimental — accuracy not yet measuredATTAC was not induced in peripheral blood T lymphocytes that robustly engage endogenous p16Ink4a with aging without concomitant expression of multiple senescence markers.
“ATTAC was also not induced in peripheral blood T lymphocytes that robustly engage endogenous p16 Ink4a with aging without concomitant expression of multiple senescence markers 2 , 13 (Extended Data Fig. 2h), further implying that transgene induction is quite selective for senescence.”
From Naturally occurring p16Ink4a-positive cells shorten healthy lifespan (2016) · cites this paper as [13]
The section ‘Increased p16 INK4a expression is associated with chronological age’ reports that p16 INK4a expression in peripheral blood T lymphocytes increases with age (page unavailable). It does not address ATTAC induction or establish whether those cells express multiple senescence markers, so it supports only the aging-related p16 portion of the attributed claim. (LLM, conf=0.88)
Experimental — accuracy not yet measuredCirculating CD3+ T cells expressing p16INK4a was identified as one of the first markers linked to senescent cells that correlates with chronological ageing.
“circulating CD3+ T cells expressing p16INK4a was identified as one the first markers linked to senescent cells that correlates with chronological ageing,44,57”
From A pilot study of senolytics to improve cognition and mobility in older adults at risk for Alzheimer's disease (2025) · cites this paper as [44]
The ‘Expression of p16INK4a in human peripheral blood cells’ section identifies CD3+ T cells as the blood fraction with the highest p16INK4a expression. The ‘Increased p16INK4a expression is associated with chronological age’ section reports a strong correlation with donor age, and the Introduction links p16INK4a to aging-related loss of replicative capacity. The paper does not establish the historical claim that this was one of the first markers linked to senescent cells. (LLM, conf=0.84)
Experimental — accuracy not yet measuredT cell p16 levels increase with physical inactivity.
“T cell p16 levels have been demonstrated to increase with age20, physical inactivity20 and smoking20”
From Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial (2024) · cites this paper as [20]
T cell p16 levels are associated with plasma IL-6 levels.
“to be associated with plasma interleukin-6 (IL-6) levels (a marker of human frailty)20”
From Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial (2024) · cites this paper as [20]
T cell p16 levels increase with smoking.
“T cell p16 levels have been demonstrated to increase with age20, physical inactivity20 and smoking20”
From Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial (2024) · cites this paper as [20]
T cell p16 levels increase with age.
“T cell p16 levels have been demonstrated to increase with age20”
From Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial (2024) · cites this paper as [20]
Sensitivity of p16INK4a to senolytics has not been tested previously.
“sensitivity of it to senolytics has not been tested previously.”
From A pilot study of senolytics to improve cognition and mobility in older adults at risk for Alzheimer's disease (2025) · cites this paper as [44]
The Discussion addresses p16INK4a as an aging biomarker and mentions caloric restriction, but does not address senolytics. Searches for senolytics and treatment response found no passage saying whether p16INK4a sensitivity to senolytics had previously been tested. Page numbers are unavailable in our copy. (LLM, conf=0.72)
Experimental — accuracy not yet measuredTime-dependent accumulation of senescent cells, likely through decreased immunoclearance, occurs in virtually all vertebrates.
“However, time-dependent accumulation of senescent cells, likely through decreased immunoclearance, occurs in virtually all vertebrates (Jeyapalan et al., 2007; Liu et al., 2009) and has been definitively shown to drive aging (Baker et al., 2016), rather than simply occur with aging.”
From DNA damage-how and why we age? (2021) · cites this paper as Liu et al., 2009
Senescent cells accumulate exponentially with ageing in different organs and tissues in model organisms and humans.
“Studies have shown that senescent cells accumulate exponentially with ageing in different organs and tissues, both in model organisms and in humans97–100.”
From Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty (2018) · cites this paper as [99]
p16 levels positively associate with age in T cells.
“p16 levels also positively associate with age in this cell type (Liu et al, 2009).”
From The struggle of a good friend getting old: cellular senescence in viral responses and therapy (2021) · cites this paper as Liu et al, 2009
P53 can cause cellular senescence by regulating the cell cycle via inhibition of CDK4 and CDK6.
“P53 can cause cellular senescence [42] by regulating the cell cycle via inhibition of cyclin-dependent kinase (CDK) 4 and CDK6 [5, 43] (Fig. 2).”
From Immunosenescence: a key player in cancer development (2020) · cites this paper as [43]
Cellular senescence is associated with expression of p16(INK4a), a protein that inhibits replication and is a biomarker of human aging.
“Cellular senescence, commonly reached by cell replication (eg, critically short telomeres) or excess cell stress (eg, DNA damage) (Blackburn, 2000,Campisi andd'Adda di Fagagna, 2007) is associated with the expression of p16(INK4a), a protein that inhibits cells from replicating (ie, a potent biomarker of human aging) (Liu et al, 2009).”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Liu et al, 2009
In 170 healthy participants aged 18-80 yr, those with more than 240 min a month of habitual physical activity had lower expression levels of P16 in circulating T cells than those who did not.
“A study of 170 healthy participants aged 18–80 yr found that those with more than 240 min a month of habitual physical activity had lower expression levels of P16 in circulating T cells than those who did not (60).”
From Exercise Counters the Age-Related Accumulation of Senescent Cells (2022) · cites this paper as [60]
Early T-lymphoid progenitors are exquisitely dependent on CDK4/6 activity.
“early T-lymphoid progenitors are exquisitely dependent on CDK4/6 activity”
From Total body irradiation causes long-term mouse BM injury via induction of HSC premature senescence in an Ink4a- and Arf-independent manner (2014) · cites this paper as [42]
Upregulation of p16 and Arf has been implicated in mediating induction of HSC senescence in a variety of pathological conditions and during aging.
“upregulation of p16 and Arf has been implicated in mediating induction of HSC senescence in a variety of pathological conditions and during aging,8,41,42”
From Total body irradiation causes long-term mouse BM injury via induction of HSC premature senescence in an Ink4a- and Arf-independent manner (2014) · cites this paper as [42]
Early T-lymphoid progenitors are very sensitive to p16 upregulation for induction of senescence during aging.
“are very sensitive to p16 upregulation for induction of senescence during aging.42,43”
From Total body irradiation causes long-term mouse BM injury via induction of HSC premature senescence in an Ink4a- and Arf-independent manner (2014) · cites this paper as [42]
Levels of p16 expression in circulating T-cells, which exhibit a strong correlation with chronological age, are inversely associated with self-reported levels of physical activity in humans.
“Levels of p16 expression in circulating T-cells, which exhibit a strong correlation with chronological age, are inversely associated with self-reported levels of physical activity in humans (Liu et al., 2009).”
From Skeletal muscle aging, cellular senescence, and senotherapeutics: current knowledge and future directions (2021) · cites this paper as Liu et al., 2009
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Cites
Estimating the Dimension of a Model
Schwarz, G. (1978) · The Annals of Statistics · doi:10.1214/aos/1176344136 · Cited by 47,033 · see citing works
Information Theory and an Extension of the Maximum Likelihood Principle
Akaike, H. (1998) · Springer series in statistics · doi:10.1007/978-1-4612-1694-0_15 · Cited by 18,384 · see citing works
Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls
The Wellcome Trust Case Control Consortium, Management Committee, Burton, P. R., Clayton, D. G., Cardon, L. R., Craddock, N., Deloukas, P., Duncanson, A., Kwiatkowski, D. P., McCarthy, M. I., et al. (2007) · Nature · doi:10.1038/nature05911 · Cited by 9,442 · see citing works
Genome-wide association analysis identifies loci for type 2 diabetes and triglyceride levels
Saxena, R., Voight, B. F., Lyssenko, V., Burtt, N. P., de Bakker, P. I. W., Chen, H., Roix, J. J., Kathiresan, S., Hirschhorn, J. N., Daly, M. J., et al. (2007) · Science · doi:10.1126/science.1142358 · Cited by 2,843 · see citing works
A genome-wide association study of type 2 diabetes in Finns detects multiple susceptibility variants
Scott, L. J., Mohlke, K. L., Bonnycastle, L. L., Willer, C. J., Li, Y., Duren, W. L., Erdos, M. R., Stringham, H. M., Chines, P. S., Jackson, A. U., et al. (2007) · Science · doi:10.1126/science.1142382 · Cited by 2,753 · see citing works
The Wellcome Trust Case Control Consortium, U.K.
Mossman, K. (2008) · Scientific American · doi:10.1038/scientificamerican0108-42a · Cited by 2,714 · see citing works
Replication of Genome-Wide Association Signals in UK Samples Reveals Risk Loci for Type 2 Diabetes
Zeggini, E., Weedon, M. N., Lindgren, C. M., Frayling, T. M., Elliott, K. S., Lango, H., Timpson, N. J., Perry, J. R. B., Rayner, N. W., Freathy, R. M., et al. (2007) · Science · doi:10.1126/science.1142364 · Cited by 2,194 · see citing works
Oncogene-Induced Senescence Relayed by an Interleukin-Dependent Inflammatory Network
Kuilman, T., Michaloglou, C., Vredeveld, L. C. W., Douma, S., van Doorn, R., Desmet, C. J., Aarden, L. A., Mooi, W. J., & Peeper, D. S. (2008) · Cell · doi:10.1016/j.cell.2008.03.039 · Cited by 2,086 · cited 1× · see citing works
“…p16INK4a expression in PBTL with aging, we investi- gated its correlation with plasma levels of IL-6, which has been reproducibly associated with cellular senescence (Coppe et al., 2008; Kuilman et al., 2008) in vitro as well as frailty and aging in vivo (reviewed in (Ershler & Keller, 2000)).”
BackgroundGenomewide Association Analysis of Coronary Artery Disease
Samani, N. J., Erdmann, J., Hall, A. S., Hengstenberg, C., Mangino, M., Mayer, B., Dixon, R. J., Meitinger, T., Braund, P., Wichmann, H.-E., et al. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa072366 · Cited by 2,044 · see citing works
A Common Variant on Chromosome 9p21 Affects the Risk of Myocardial Infarction
Helgadottir, A., Thorleifsson, G., Manolescu, A., Gretarsdottir, S., Blondal, T., Jonasdottir, A., Jonasdottir, A., Sigurdsson, A., Baker, A., Palsson, A., et al. (2007) · Science · doi:10.1126/science.1142842 · Cited by 1,594 · see citing works
A Common Allele on Chromosome 9 Associated with Coronary Heart Disease
McPherson, R., Pertsemlidis, A., Kavaslar, N., Stewart, A., Roberts, R., Cox, D. R., Hinds, D. A., Pennacchio, L. A., Tybjaerg-Hansen, A., Folsom, A. R., et al. (2007) · Science · doi:10.1126/science.1142447 · Cited by 1,587 · see citing works
Tumor Suppression at the Mouse INK4a Locus Mediated by the Alternative Reading Frame Product p19
Kamijo, T., Zindy, F., Roussel, M. F., Quelle, D. E., Downing, J. R., Ashmun, R. A., Grosveld, G., & Sherr, C. J. (1997) · Cell · doi:10.1016/s0092-8674(00)80452-3 · Cited by 1,566 · see citing works
Ink4a/Arf expression is a biomarker of aging
Krishnamurthy, J., Torrice, C., Ramsey, M. R., Kovalev, G. I., Al-Regaiey, K., Su, L., & Sharpless, N. E. (2004) · Journal of Clinical Investigation · doi:10.1172/jci22475 · Cited by 1,486 · see citing works
Self-citationObesity, cigarette smoking, and telomere length in women
Valdes, A., Andrew, T., Gardner, J., Kimura, M., Oelsner, E., Cherkas, L., Aviv, A., & Spector, T. (2005) · The Lancet · doi:10.1016/s0140-6736(05)66630-5 · Cited by 1,363 · see citing works
Telomerase Mutations in Families with Idiopathic Pulmonary Fibrosis
Armanios, M. Y., Chen, J. J.-L., Cogan, J. D., Alder, J. K., Ingersoll, R. G., Markin, C., Lawson, W. E., Xie, M., Vulto, I., Phillips, J. A., et al. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa066157 · Cited by 1,357 · see citing works
Age-Associated Increased Interleukin-6 Gene Expression, Late-Life Diseases, and Frailty
Ershler, W. B., & Keller, E. T. (2000) · Annual Review of Medicine · doi:10.1146/annurev.med.51.1.245 · Cited by 1,282 · see citing works
Stem-cell ageing modified by the cyclin-dependent kinase inhibitor p16INK4a
Janzen, V., Forkert, R., Fleming, H. E., Saito, Y., Waring, M. T., Dombkowski, D. M., Cheng, T., DePinho, R. A., Sharpless, N. E., & Scadden, D. T. (2006) · Nature · doi:10.1038/nature05159 · Cited by 1,106 · see citing works
Self-citationCellular Senescence in Aging Primates
Herbig, U., Ferreira, M., Condel, L., Carey, D., & Sedivy, J. M. (2006) · Science · doi:10.1126/science.1122446 · Cited by 1,101 · see citing works
The Regulation of INK4/ARF in Cancer and Aging
Kim, W. Y., & Sharpless, N. E. (2006) · Cell · doi:10.1016/j.cell.2006.10.003 · Cited by 1,009 · see citing works
Self-citationp16INK4a induces an age-dependent decline in islet regenerative potential
Krishnamurthy, J., Ramsey, M. R., Ligon, K. L., Torrice, C., Koh, A., Bonner-Weir, S., & Sharpless, N. E. (2006) · Nature · doi:10.1038/nature05092 · Cited by 1,003 · cited 4× · see citing works
“…an attenuated decline in the replicative capacity of several self-renewing compartments has been observed, including hematopoietic stem cells (Janzen et al., 2006), pancreatic b-cells (Krishnamurthy et al., 2006), neural stem cells (Molofsky et al., 2006) and B-lymphocytes (Signer et al., 2008).”
BackgroundInfluentialSelf-citationThe common biology of cancer and ageing
Finkel, T., Serrano, M., & Blasco, M. A. (2007) · Nature · doi:10.1038/nature05985 · Cited by 988 · see citing works
Increasing p16INK4a expression decreases forebrain progenitors and neurogenesis during ageing
Molofsky, A. V., Slutsky, S. G., Joseph, N. M., He, S., Pardal, R., Krishnamurthy, J., Sharpless, N. E., & Morrison, S. J. (2006) · Nature · doi:10.1038/nature05091 · Cited by 972 · cited 4× · see citing works
“…an attenuated decline in the replicative capacity of several self-renewing compartments has been observed, including hematopoietic stem cells (Janzen et al., 2006), pancreatic b-cells (Krishnamurthy et al., 2006), neural stem cells (Molofsky et al., 2006) and B-lymphocytes (Signer et al., 2008).”
BackgroundInfluentialSelf-citationBracken, A. P., Kleine-Kohlbrecher, D., Dietrich, N., Pasini, D., Gargiulo, G., Beekman, C., Theilgaard-Mönch, K., Minucci, S., Porse, B. T., Marine, J.-C., et al. (2007) · Genes & Development · doi:10.1101/gad.415507 · Cited by 850 · see citing works
Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis
Sharpless, N. E., Bardeesy, N., Lee, K.-H., Carrasco, D., Castrillon, D. H., Aguirre, A. J., Wu, E. A., Horner, J. W., & DePinho, R. A. (2001) · Nature · doi:10.1038/35092592 · Cited by 848 · see citing works
Self-citationThe Influence of Age on T Cell Generation and TCR Diversity
Naylor, K., Li, G., Vallejo, A. N., Lee, W.-W., Koetz, K., Bryl, E., Witkowski, J., Fulbright, J., Weyand, C. M., & Goronzy, J. J. (2005) · The Journal of Immunology · doi:10.4049/jimmunol.174.11.7446 · Cited by 802 · see citing works
Loss of telomeric DNA during aging of normal and trisomy 21 human lymphocytes.
Vaziri, H., Schächter, F., Uchida, I. A., Wei, L., Zhu, X., Effros, R. B., Cohen, D., & Harley, C. (1993) · PubMed · Cited by 734 · see citing works
Helgadóttir, A., Þorleifsson, G., Magnússon, K. P., Grétarsdóttir, S., Steinthórsdóttir, V., Manolescu, A. R., Jones, G. T., Rinkel, G. J. E., Blankensteijn, J. D., Ronkainen, A., et al. (2008) · Nature Genetics · doi:10.1038/ng.72 · Cited by 724 · see citing works
Rufer, N., Brümmendorf, T. H., Kolvraa, S., Bischoff, C., Christensen, K., Wadsworth, L., Schulzer, M., & Lansdorp, P. M. (1999) · The Journal of Experimental Medicine · doi:10.1084/jem.190.2.157 · Cited by 709 · see citing works
The rate of telomere sequence loss in human leukocytes varies with age
Frenck, R. W., Blackburn, E. H., & Shannon, K. M. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.10.5607 · Cited by 675 · see citing works
Pasmant, É., Laurendeau, I., Héron, D., Vidaud, M., Vidaud, D., & Bièche, I. (2007) · Cancer Research · doi:10.1158/0008-5472.can-06-2004 · Cited by 618 · see citing works
Zindy, F., Quelle, D. E., Roussel, M. F., & Sherr, C. J. (1997) · Oncogene · doi:10.1038/sj.onc.1201178 · Cited by 574 · see citing works
Telomere Shortening Is Associated with Cell Division in Vitro and in Vivo
Allsopp, R. C., Chang, E., Kashefi-Aazam, M., Rogaev, E. I., Piatyszek, M. A., Shay, J. W., & Harley, C. B. (1995) · Experimental Cell Research · doi:10.1006/excr.1995.1306 · Cited by 533 · see citing works
A Common Allele on Chromosome 9 Associated With Coronary Heart Disease
McPherson, R., Pertsemlidis, A., Kavaslar, N., Stewart, A. F. R., Roberts, R., Cox, D., Hinds, D. A., Pennacchio, L. A., Tybjærg‐Hansen, A., Folsom, A. R., et al. (2007) · Obstetrical & Gynecological Survey · doi:10.1097/01.ogx.0000279314.45442.bb · Cited by 524 · see citing works
Cancer and ageing: rival demons?
Campisi, J. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1073 · Cited by 512 · cited 2× · see citing works
“activation of tumor suppressor mechanisms such as telomere dysfunction and p16 activation (Campisi, 2003; Kim & Sharpless, 2006; Finkel et al., 2007).”
BackgroundBroadbent, H. M., Peden, J. F., Stefan Lorkowski, A., Goel, A., Ongen, H., Green, F. R., Clarke, R., Collins, R., Franzosi, M. G., Tognoni, G., et al. (2007) · Human Molecular Genetics · doi:10.1093/hmg/ddm352 · Cited by 504 · see citing works
Huster, K. M., Busch, V., Schiemann, M., Linkemann, K., Kerksiek, K. M., Wagner, H., & Busch, D. H. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0308054101 · Cited by 474 · see citing works
Opposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency
Baker, D. J., Perez-Terzic, C., Jin, F., Pitel, K. S., Niederländer, N. J., Jeganathan, K., Yamada, S., Reyes, S., Rowe, L., Hiddinga, H. J., et al. (2008) · Nature Cell Biology · doi:10.1038/ncb1744 · Cited by 408 · cited 4× · see citing works
“Moreover, inactivation of p16INK4a, but not Arf, partially rescues several age-related phenotypes in a progeroid mouse strain (Baker et al., 2008).”
BackgroundInfluentialChen, H., Gu, X., Su, I.-H., Bottino, R., Contreras, J. L., Tarakhovsky, A., & Kim, S. K. (2009) · Genes & Development · doi:10.1101/gad.1742509 · Cited by 366 · see citing works
Melk, A., Schmidt, B. M. W., Takeuchi, O., Sawitzki, B., Rayner, D. C., & Halloran, P. F. (2004) · Kidney International · doi:10.1111/j.1523-1755.2004.00438.x · Cited by 362 · see citing works
Alter, B. P., Baerlocher, G. M., Savage, S. A., Chanock, S. J., Weksler, B. B., Willner, J. P., Peters, J. A., Giri, N., & Lansdorp, P. M. (2007) · Blood · doi:10.1182/blood-2007-02-075598 · Cited by 356 · see citing works
Cutting Edge: Increased Expression of Bcl-2 in Antigen-Specific Memory CD8+ T Cells
Grayson, J. M., Zajac, A. J., Altman, J. D., & Ahmed, R. (2000) · The Journal of Immunology · doi:10.4049/jimmunol.164.8.3950 · Cited by 349 · see citing works
Incomplete Data in Generalized Linear Models
Ibrahim, J. G. (1990) · Journal of the American Statistical Association · doi:10.1080/01621459.1990.10474938 · Cited by 321 · see citing works
Self-citationKotake, Y., Cao, R., Viatour, P., Sage, J., Zhang, Y., & Xiong, Y. (2007) · Genes & Development · doi:10.1101/gad.1499407 · Cited by 314 · see citing works
Coppé, J.-P., Patil, C. K., Rodier, F., Sun, Y., Muñoz, D. P., Goldstein, J., Nelson, P. S., Desprez, P.-Y., & Campisi, J. (2008) · PLoS Biology · doi:10.1371/journal.pbio.0060301 · Cited by 302 · cited 2× · see citing works
“gated its correlation with plasma levels of IL-6, which has been reproducibly associated with cellular senescence (Coppe et al., 2008; Kuilman et al., 2008) in vitro as well as frailty and aging in vivo (reviewed in (Ershler & Keller, 2000)).”
BackgroundINK4/ARF transcript expression is associated with chromosome 9p21 variants linked to atherosclerosis
Liu, Y., Sanoff, H. K., Cho, H., Burd, C. E., Torrice, C., Mohlke, K. L., Ibrahim, J. G., Thomas, N. E., & Sharpless, N. E. (2009) · PLoS ONE · doi:10.1371/journal.pone.0005027 · Cited by 248 · see citing works
Self-citationUtsuyama, M., Hirokawa, K., Kurashima, C., Fukayama, M., Inamatsu, T., Suzuki, K., Hashimoto, W., & Sato, K. (1992) · Mechanisms of Ageing and Development · doi:10.1016/0047-6374(92)90016-7 · Cited by 239 · see citing works
Role of p14<sup>ARF</sup> in Replicative and Induced Senescence of Human Fibroblasts
Wei, W., Hemmer, R. M., & Sedivy, J. M. (2001) · Molecular and Cellular Biology · doi:10.1128/mcb.21.20.6748-6757.2001 · Cited by 217 · see citing works
Paoli, P. D., Battistin, S., & Santini, G. F. (1988) · Clinical Immunology and Immunopathology · doi:10.1016/0090-1229(88)90022-0 · Cited by 213 · see citing works
Melk, A., Kittikowit, W., Sandhu, I., Halloran, K. M., Grimm, P., Schmidt, B. M. W., & Halloran, P. F. (2003) · Kidney International · doi:10.1046/j.1523-1755.2003.00032.x · Cited by 205 · see citing works
Son, N. H., Murray, S., Yanovski, J., Hodes, R. J., & Weng, N.-P. (2000) · The Journal of Immunology · doi:10.4049/jimmunol.165.3.1191 · Cited by 200 · see citing works
Gene expression profiling of aging reveals activation of a p53-mediated transcriptional program
Edwards, M. G., Anderson, R. M., Yuan, M., Kendziorski, C. M., Weindruch, R., & Prolla, T. A. (2007) · BMC Genomics · doi:10.1186/1471-2164-8-80 · Cited by 174 · see citing works
Immunohistochemical survey of p16INK4A expression in normal human adult and infant tissues.
Nielsen, G. P., Stemmer-Rachamimov, A. O., Shaw, J., Roy, J. E., Koh, J., & Louis, D. N. (1999) · PubMed · Cited by 169 · see citing works
Matarín, M., Brown, W. M., Singleton, A., Hardy, J., & Meschia, J. F. (2008) · Stroke · doi:10.1161/strokeaha.107.502963 · Cited by 168 · see citing works
Markers of cellular senescence in zero hour biopsies predict outcome in renal transplantation
Koppelstaetter, C., Schratzberger, G., Perco, P., Hofer, J., Mark, W., Öllinger, R., Oberbauer, R., Schwarz, C., Mitterbauer, C., Kainz, A., et al. (2008) · Aging Cell · doi:10.1111/j.1474-9726.2008.00398.x · Cited by 124 · see citing works
Cellular senescence in pretransplant renal biopsies predicts postoperative organ function
McGlynn, L. M., Stevenson, K. S., Lamb, K. J., Zino, S., Brown, M., Prina, A., Kingsmore, D. B., & Shiels, P. G. (2008) · Aging Cell · doi:10.1111/j.1474-9726.2008.00447.x · Cited by 108 · see citing works
Signer, R. A. J., Montecino-Rodriguez, E., Witte, O. N., & Dorshkind, K. (2008) · Genes & Development · doi:10.1101/gad.1715808 · Cited by 102 · see citing works
Munro, J., Stott, F. J., Vousden, K. H., Peters, G., & Parkinson, E. K. (1999) · PubMed · Cited by 93 · see citing works
A common variant of the p16INK4a genetic region is associated with physical function in older people
Melzer, D., Frayling, T. M., Murray, A., Hurst, A. J., Harries, L. W., Song, H., Khaw, K., Luben, R., Surtees, P. G., Bandinelli, S. S., et al. (2007) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2007.03.005 · Cited by 84 · see citing works
Shields, J. M., Thomas, N. E., Cregger, M. A., Berger, A. J., Leslie, M. C., Torrice, C., Hao, H., Penland, S., Arbiser, J. L., Scott, G., et al. (2007) · Cancer Research · doi:10.1158/0008-5472.can-06-3311 · Cited by 81 · see citing works
Self-citationAge-related defects in B lymphopoiesis underlie the myeloid dominance of adult leukemia
Signer, R. A. J., Montecino-Rodriguez, E., Witte, O. N., McLaughlin, J., & Dorshkind, K. (2007) · Blood · doi:10.1182/blood-2007-01-069401 · Cited by 77 · see citing works
Zhang, N., & He, Y.-W. (2005) · The Journal of Immunology · doi:10.4049/jimmunol.174.11.6967 · Cited by 60 · see citing works
Flagged first, then by citations
Research works printed but not linked: 2
- [18]18. Helgadottir A, Thorleifsson G, Magnusson KP, Gretarsdottir S, Stein- thorsdottir V, Manolescu A, Jones GT, Rinkel GJ, Blankensteijn JD, Ronkainen A, Jaaskelainen JE, Kyo Y, Lenk GM, Sakalihasan N, Kos- tulas K, Gottsater A, Flex A, Stefansson H, Hansen T, Andersen G, Weinsheimer S, Borch-Johnsen K, Jorgensen T, Shah SH, Quyyumi AA, Granger CB, Reilly MP, Austin H, Levey AI, Vaccarino V, Pals- dottir E, Walters GB, Jonsdottir T, Snorradottir S, Magnusdottir D, Gudmundsson G, Ferrell RE, Sveinbjornsdottir S, Hernesniemi J, Niemela M, Limet R, Andersen K, Sigurdsson G, Benediktsson R, Verhoeven EL, Teijink JA, Grobbee DE, Rader DJ, Collier DA, Peder- sen O, Pola R, Hillert J, Lindblad B, Valdimarsson EM, Magnadottir p16 INK4a in human aging, Y. Liu et al. ª 2009 The Authors Journal compilation ª Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland 2009
- [47]47. Scott LJ, Mohlke KL, Bonnycastle LL, Willer CJ, Li Y, Duren WL, Erdos MR, Stringham HM, Chines PS, Jackson AU, Prokunina-Olsson L, Ding CJ, Swift AJ, Narisu N, Hu T, Pruim R, Xiao R, Li XY, Conneely KN, p16 INK4a in human aging, Y. Liu et al. ª 2009 The Authors Journal compilation ª Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland 2009
Cited by
Sorted by citations
Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty
Ferrucci, L., & Fabbri, E. (2018) · Nature Reviews Cardiology · doi:10.1038/s41569-018-0064-2 · Cited by 3,690 · see citing works
Aging, Cellular Senescence, and Cancer
Campisi, J. (2013) · Annual Review of Physiology · doi:10.1146/annurev-physiol-030212-183653 · Cited by 2,954 · see citing works
Naturally occurring p16Ink4a-positive cells shorten healthy lifespan
Baker, D. J., Childs, B. G., Durik, M., Wijers, M. E., Sieben, C. J., Zhong, J., A. Saltness, R., Jeganathan, K. B., Verzosa, G. C., Pezeshki, A., et al. (2016) · Nature · doi:10.1038/nature16932 · Cited by 2,891 · see citing works
Four faces of cellular senescence
Rodier, F., & Campisi, J. (2011) · Journal of Cell Biology · doi:10.1083/jcb.201009094 · Cited by 2,016 · see citing works
“Several years ago, two landmark papers described mouse models in which constitutive expression of an artificially (Tyner et al., 2002) or naturally (Maier et al., 2004) truncated p53 protein resulted in chronically elevated p53 activity.”
Senescence in Health and Disease
He, S., & Sharpless, N. E. (2017) · Cell · doi:10.1016/j.cell.2017.05.015 · Cited by 1,766 · see citing works
Self-citationCellular senescence promotes adverse effects of chemotherapy and cancer relapse
Demaria, M., O'Leary, M. N., Chang, J., Shao, L., Liu, S., Alimirah, F., Koenig, K., Le, C., Mitin, N., Deal, A. M., et al. (2017) · Cancer Discovery · doi:10.1158/2159-8290.cd-16-0241 · Cited by 1,338 · see citing works
Self-citationCellular Senescence: Aging, Cancer, and Injury
Calcinotto, A., Kohli, J., Zagato, E., Pellegrini, L., Demaria, M., & Alimonti, A. (2019) · Physiological Reviews · doi:10.1152/physrev.00020.2018 · Cited by 1,270 · see citing works
Forging a signature of in vivo senescence
Sharpless, N. E., & Sherr, C. J. (2015) · Nature Reviews Cancer · doi:10.1038/nrc3960 · Cited by 1,104 · see citing works
Self-citationFisetin is a senotherapeutic that extends health and lifespan
Yousefzadeh, M. J., Zhu, Y., McGowan, S. J., Angelini, L., Fuhrmann-Stroissnigg, H., Xu, M., Ling, Y. Y., Melos, K. I., Pirtskhalava, T., Inman, C. L., et al. (2018) · EBioMedicine · doi:10.1016/j.ebiom.2018.09.015 · Cited by 1,032 · see citing works
Self-citationAn aged immune system drives senescence and ageing of solid organs
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., et al. (2021) · Nature · doi:10.1038/s41586-021-03547-7 · Cited by 972 · see citing works
Self-citationMeasuring biological aging in humans: a quest
Ferrucci, L., Gonzalez‐Freire, M., Fabbri, E., Simonsick, E., Tanaka, T., Moore, Z., Salimi, S., Sierra, F., & de Cabo, R. (2020) · Aging Cell · doi:10.1111/acel.13080 · Cited by 781 · see citing works
Sleep health: Reciprocal regulation of sleep and innate immunity
Irwin, M. R., & Opp, M. R. (2017) · Neuropsychopharmacology · doi:10.1038/npp.2016.148 · Cited by 624 · see citing works
Plasma proteomic signature of age in healthy humans
Tanaka, T., Biancotto, A., Moaddel, R., Moore, A. Z., Gonzalez‐Freire, M., Aon, M. A., Candia, J., Zhang, P., Cheung, F., Fantoni, G., et al. (2018) · Aging Cell · doi:10.1111/acel.12799 · Cited by 562 · see citing works
Mechanisms underlying T cell ageing
Goronzy, J. J., & Weyand, C. M. (2019) · Nature Reviews Immunology · doi:10.1038/s41577-019-0180-1 · Cited by 506 · see citing works
Immunosenescence: a key player in cancer development
Lian, J., Yue, Y., Yu, W., & Zhang, Y. (2020) · Journal of Hematology & Oncology · doi:10.1186/s13045-020-00986-z · Cited by 510 · see citing works
Monitoring Tumorigenesis and Senescence In Vivo with a p16INK4a-Luciferase Model
Burd, C. E., Sorrentino, J. A., Clark, K. S., Darr, D. B., Krishnamurthy, J., Deal, A. M., Bardeesy, N., Castrillon, D. H., Beach, D. H., & Sharpless, N. E. (2013) · Cell · doi:10.1016/j.cell.2012.12.010 · Cited by 419 · see citing works
Self-citationCellular senescence: a link between cancer and age-related degenerative disease?
Campisi, J., Andersen, J. K., Kapahi, P., & Melov, S. (2011) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2011.09.001 · Cited by 421 · see citing works
Exercise Attenuates the Major Hallmarks of Aging
Garatachea, N., Pareja-Galeano, H., Sanchis-Gomar, F., Santos-Lozano, A., Fiuza-Luces, C., Morán, M., Emanuele, E., Joyner, M. J., & Lucia, A. (2015) · Rejuvenation Research · doi:10.1089/rej.2014.1623 · Cited by 413 · see citing works
DNA damage checkpoints in stem cells, ageing and cancer
Sperka, T., Wang, J., & Rudolph, K. L. (2012) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3420 · Cited by 393 · see citing works
SenNet recommendations for detecting senescent cells in different tissues
Suryadevara, V., Hudgins, A. D., Rajesh, A., Pappalardo, A., Karpova, A., Dey, A. K., Hertzel, A., Agudelo, A., Rocha, A., Soygur, B., et al. (2024) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-024-00738-8 · Cited by 408 · see citing works
“…that as CDKN2A -expressing peripheral mononuclear blood cells do not appear to survive cryopreservation, quantitative PCR (qPCR) assays that quantify CDKN2A mRNA levels in peripheral T cells have mainly used CD3 + cells isolated from fresh blood to ensure representation of the senescent subset 88 .”
DNA damage-how and why we age?
Yousefzadeh, M., Henpita, C., Vyas, R., Soto-Palma, C., Robbins, P., & Niedernhofer, L. (2021) · eLife · doi:10.7554/elife.62852 · Cited by 399 · see citing works
Guidelines for minimal information on cellular senescence experimentation in vivo
Ogrodnik, M., Carlos Acosta, J., Adams, P. D., d’Adda di Fagagna, F., Baker, D. J., Bishop, C. L., Chandra, T., Collado, M., Gil, J., Gorgoulis, V., et al. (2024) · Cell · doi:10.1016/j.cell.2024.05.059 · Cited by 376 · see citing works
microRNA Expression Patterns Reveal Differential Expression of Target Genes with Age
Noren Hooten, N., Abdelmohsen, K., Gorospe, M., Ejiogu, N., Zonderman, A. B., & Evans, M. K. (2010) · PLoS ONE · doi:10.1371/journal.pone.0010724 · Cited by 357 · see citing works
The flavonoid procyanidin C1 has senotherapeutic activity and increases lifespan in mice
Xu, Q., Fu, Q., Li, Z., Liu, H., Wang, Y., Lin, X., He, R., Zhang, X., Ju, Z., Campisi, J., et al. (2021) · Nature Metabolism · doi:10.1038/s42255-021-00491-8 · Cited by 341 · see citing works
Tissue specificity of senescent cell accumulation during physiologic and accelerated aging of mice
Yousefzadeh, M. J., Zhao, J., Bukata, C., Wade, E. A., McGowan, S. J., Angelini, L. A., Bank, M. P., Gurkar, A. U., McGuckian, C. A., Calubag, M. F., et al. (2020) · Aging Cell · doi:10.1111/acel.13094 · Cited by 331 · see citing works
Self-citationLiu, J.-Y., Souroullas, G. P., Diekman, B. O., Krishnamurthy, J., Hall, B. M., Sorrentino, J. A., Parker, J. S., Sessions, G. A., Gudkov, A. V., & Sharpless, N. E. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1818313116 · Cited by 306 · see citing works
Self-citationEffect of Cytotoxic Chemotherapy on Markers of Molecular Age in Patients With Breast Cancer
Sanoff, H. K., Deal, A. M., Krishnamurthy, J., Torrice, C., Dillon, P., Sorrentino, J., Ibrahim, J. G., Jolly, T. A., Williams, G., Carey, L. A., et al. (2014) · JNCI: Journal of the National Cancer Institute · doi:10.1093/jnci/dju057 · Cited by 283 · see citing works
Self-citationMarkers of T Cell Senescence in Humans
Xu, W., & Larbi, A. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18081742 · Cited by 261 · see citing works
Exercise sustains the hallmarks of health
Qiu, Y., Fernández-García, B., Lehmann, H. I., Li, G., Kroemer, G., López-Otín, C., & Xiao, J. (2023) · Journal of Sport and Health Science · doi:10.1016/j.jshs.2022.10.003 · Cited by 270 · see citing works
The number of p16INK4a positive cells in human skin reflects biological age
Waaijer, M. E. C., Parish, W. E., Strongitharm, B. H., van Heemst, D., Slagboom, P. E., de Craen, A. J. M., Sedivy, J. M., Westendorp, R. G. J., Gunn, D. A., & Maier, A. B. (2012) · Aging Cell · doi:10.1111/j.1474-9726.2012.00837.x · Cited by 264 · see citing works
Martínez‐Zamudio, R. I., Dewald, H. K., Vasilopoulos, T., Gittens‐Williams, L., Fitzgerald‐Bocarsly, P., & Herbig, U. (2021) · Aging Cell · doi:10.1111/acel.13344 · Cited by 213 · see citing works
Spontaneous DNA damage to the nuclear genome promotes senescence, redox imbalance and aging
Robinson, A. R., Yousefzadeh, M. J., Rozgaja, T. A., Wang, J., Li, X., Tilstra, J. S., Feldman, C. H., Gregg, S. Q., Johnson, C. H., Skoda, E. M., et al. (2018) · Redox Biology · doi:10.1016/j.redox.2018.04.007 · Cited by 155 · see citing works
Self-citationLe, O. N. L., Rodier, F., Fontaine, F., Coppe, J., Campisi, J., DeGregori, J., Laverdière, C., Kokta, V., Haddad, E., & Beauséjour, C. M. (2010) · Aging Cell · doi:10.1111/j.1474-9726.2010.00567.x · Cited by 168 · see citing works
Senescent cell turnover slows with age providing an explanation for the Gompertz law
Karin, O., Agrawal, A., Porat, Z., Krizhanovsky, V., & Alon, U. (2019) · Nature Communications · doi:10.1038/s41467-019-13192-4 · Cited by 151 · see citing works
Diekman, B. O., Sessions, G. A., Collins, J. A., Knecht, A. K., Strum, S. L., Mitin, N. K., Carlson, C. S., Loeser, R. F., & Sharpless, N. E. (2018) · Aging Cell · doi:10.1111/acel.12771 · Cited by 158 · see citing works
Self-citationShao, L., Feng, W., Li, H., Gardner, D., Luo, Y., Wang, Y., Liu, L., Meng, A., Sharpless, N. E., & Zhou, D. (2014) · Blood · doi:10.1182/blood-2013-07-515619 · Cited by 165 · see citing works
Self-citationSong, Z., Von Figura, G., Liu, Y., Kraus, J. M., Torrice, C., Dillon, P., Rudolph‐Watabe, M., Ju, Z., Kestler, H. A., Sanoff, H., et al. (2010) · Aging Cell · doi:10.1111/j.1474-9726.2010.00583.x · Cited by 163 · see citing works
Self-citationShiels, P. G., McGlynn, L. M., MacIntyre, A., Johnson, P. C. D., Batty, G. D., Burns, H., Cavanagh, J., Deans, K. A., Ford, I., McConnachie, A., et al. (2011) · PLoS ONE · doi:10.1371/journal.pone.0022521 · Cited by 143 · see citing works
Psychosocial stressors and telomere length: A current review of the science
Rentscher, K. E., Carroll, J. E., & Mitchell, C. (2020) · Annual Review of Public Health · doi:10.1146/annurev-publhealth-040119-094239 · Cited by 138 · see citing works
SenNet Consortium, Writing Group, Lee, P. J., Benz, C. C., Blood, P., Börner, K., Campisi, J., Chen, F., Daldrup-Link, H., De Jager, P., et al. (2022) · Nature Aging · doi:10.1038/s43587-022-00326-5 · Cited by 122 · see citing works
Carroll, J. E., Cole, S. W., Seeman, T. E., Breen, E. C., Witarama, T., Arevalo, J. M. G., Ma, J., & Irwin, M. R. (2016) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2015.08.024 · Cited by 129 · see citing works
Role of Cellular Senescence in Type II Diabetes
Narasimhan, A., Flores, R. R., Robbins, P. D., & Niedernhofer, L. J. (2021) · Endocrinology · doi:10.1210/endocr/bqab136 · Cited by 133 · see citing works
Justice, J. N., Gregory, H., Tchkonia, T., LeBrasseur, N. K., Kirkland, J. L., Kritchevsky, S. B., & Nicklas, B. J. (2018) · The Journals of Gerontology: Series A · doi:10.1093/gerona/glx134 · Cited by 129 · see citing works
Exercise reduces circulating biomarkers of cellular senescence in humans
Englund, D. A., Sakamoto, A. E., Fritsche, C. M., Heeren, A. A., Zhang, X., Kotajarvi, B. R., Lecy, D. R., Yousefzadeh, M. J., Schafer, M. J., White, T. A., et al. (2021) · Aging Cell · doi:10.1111/acel.13415 · Cited by 125 · see citing works
Senescent Carcinoma-Associated Fibroblasts Upregulate IL8 to Enhance Prometastatic Phenotypes
Wang, T., Notta, F., Navab, R., Joseph, J., Ibrahimov, E., Xu, J., Zhu, C.-Q., Borgida, A., Gallinger, S., & Tsao, M.-S. (2017) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-16-0192 · Cited by 123 · see citing works
Farr, J. N., Atkinson, E. J., Achenbach, S. J., Volkman, T. L., Tweed, A. J., Vos, S. J., Ruan, M., Sfeir, J., Drake, M. T., Saul, D., et al. (2024) · Nature Medicine · doi:10.1038/s41591-024-03096-2 · Cited by 127 · see citing works
Expression of p16INK4a prevents cancer and promotes aging in lymphocytes
Liu, Y., Johnson, S. M., Fedoriw, Y., Rogers, A. B., Yuan, H., Krishnamurthy, J., & Sharpless, N. E. (2011) · Blood · doi:10.1182/blood-2010-09-304402 · Cited by 114 · see citing works
Self-citationEffects of exercise on cellular and tissue aging
Carapeto, P. V., & Aguayo-Mazzucato, C. (2021) · Aging · doi:10.18632/aging.203051 · Cited by 107 · see citing works
Cellular senescence as a potential mediator of COVID‐19 severity in the elderly
Nehme, J., Borghesan, M., Mackedenski, S., Bird, T. G., & Demaria, M. (2020) · Aging Cell · doi:10.1111/acel.13237 · Cited by 94 · see citing works
Englund, D. A., Zhang, X., Aversa, Z., & LeBrasseur, N. K. (2021) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2021.111595 · Cited by 94 · see citing works
Can blocking inflammation enhance immunity during aging?
Chambers, E. S., & Akbar, A. N. (2020) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2020.03.016 · Cited by 92 · see citing works
Bacterial induction of B cell senescence promotes age-related changes in the gut microbiota
Kawamoto, S., Uemura, K., Hori, N., Takayasu, L., Konishi, Y., Katoh, K., Matsumoto, T., Suzuki, M., Sakai, Y., Matsudaira, T., et al. (2023) · Nature Cell Biology · doi:10.1038/s41556-023-01145-5 · Cited by 91 · see citing works
Parish, S. T., Wu, J. E., & Effros, R. B. (2010) · Journal of Clinical Immunology · doi:10.1007/s10875-010-9449-7 · Cited by 85 · see citing works
Is exercise a senolytic medicine? A systematic review
Chen, X., Yi, Z., Wong, G. T., Hasan, K. M. M., Kwan, J. S., Ma, A. C., & Chang, R. C. (2021) · Aging Cell · doi:10.1111/acel.13294 · Cited by 88 · see citing works
Ageing as developmental decay: insights from p16INK4a.
Martin, N., Beach, D., & Gil, J. (2014) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2014.09.008 · Cited by 76 · see citing works
Millar, C. L., Iloputaife, I., Baldyga, K., Norling, A. M., Boulougoura, A., Vichos, T., Tchkonia, T., Deisinger, A., Pirtskhalava, T., Kirkland, J. L., et al. (2025) · EBioMedicine · doi:10.1016/j.ebiom.2025.105612 · Cited by 88 · see citing works
“1 Although, circulating CD3+ T cells expressing p16 INK4a was identi fi ed as one the fi rst markers linked to senescent cells that correlates with chronological ageing, 44,57 sensitivity of it to seno-lytics has not been tested previously.”
Smitherman, A. B., Wood, W. A., Mitin, N., Ayer Miller, V. L., Deal, A. M., Davis, I. J., Blatt, J., Gold, S. H., & Muss, H. B. (2020) · Cancer · doi:10.1002/cncr.33112 · Cited by 80 · see citing works
<i>Cdkn2a</i> Is an Atherosclerosis Modifier Locus That Regulates Monocyte/Macrophage Proliferation
Kuo, C.-L., Murphy, A. J., Sayers, S., Li, R., Yvan-Charvet, L., Davis, J. Z., Krishnamurthy, J., Liu, Y., Puig, O., Sharpless, N. E., et al. (2011) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.111.234492 · Cited by 73 · see citing works
Self-citationTeyssier, J.-R., Chauvet-Gelinier, J.-C., Ragot, S., & Bonin, B. (2012) · PLoS ONE · doi:10.1371/journal.pone.0049677 · Cited by 73 · see citing works
Nelson, J. A. E., Krishnamurthy, J., Menezes, P., Liu, Y., Hudgens, M. G., Sharpless, N. E., & Eron, J. J. (2012) · Aging Cell · doi:10.1111/j.1474-9726.2012.00856.x · Cited by 66 · see citing works
Self-citationExercise Counters the Age-Related Accumulation of Senescent Cells
Zhang, X., Englund, D. A., Aversa, Z., Jachim, S. K., White, T. A., & LeBrasseur, N. K. (2022) · Exercise and Sport Sciences Reviews · doi:10.1249/jes.0000000000000302 · Cited by 63 · see citing works
Molecular pathology endpoints useful for aging studies
Niedernhofer, L. J., Kirkland, J. L., & Ladiges, W. (2017) · Ageing Research Reviews · doi:10.1016/j.arr.2016.09.012 · Cited by 59 · see citing works
The struggle of a good friend getting old: cellular senescence in viral responses and therapy
Kohli, J., Veenstra, I., & Demaria, M. (2021) · The EMBO Reports · doi:10.15252/embr.202052243 · Cited by 52 · see citing works
Identification of distinct and age‐dependent p16<sup>High</sup> microglia subtypes
Talma, N., Gerrits, E., Wang, B., Eggen, B. J. L., & Demaria, M. (2021) · Aging Cell · doi:10.1111/acel.13450 · Cited by 46 · see citing works
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 · see citing works
Pustavoitau, A., Barodka, V., Sharpless, N. E., Torrice, C., Nyhan, D., Berkowitz, D. E., Shah, A. S., Bandeen Roche, K. J., & Walston, J. D. (2016) · Experimental Gerontology · doi:10.1016/j.exger.2015.12.003 · Cited by 36 · see citing works
Self-citationBarriers to the Preclinical Development of Therapeutics that Target Aging Mechanisms: Table 1.
Burd, C. E., Gill, M. S., Niedernhofer, L. J., Robbins, P. D., Austad, S. N., Barzilai, N., & Kirkland, J. L. (2016) · The Journals of Gerontology Series A: Biological Sciences and Medical Sciences · doi:10.1093/gerona/glw112 · Cited by 28 · see citing works
Self-citationSenolytic effect of high intensity interval exercise on human skeletal muscle
Jean, W.-H., Hsieh, Y.-W., Lai, L.-F., Dewi, L., Liao, Y.-C., Ye, M., Yu, S.-H., Kao, C.-L., Huang, C.-Y., & Kuo, C.-H. (2023) · Aging · doi:10.18632/aging.204511 · Cited by 18 · see citing works
Psychiatric disorders, morbidity, and mortality: tracing mechanistic pathways to accelerated aging
Kiecolt-Glaser, J. K., & Wilson, S. J. (2016) · Psychosomatic Medicine · doi:10.1097/psy.0000000000000373 · Cited by 14 · see citing works
Chen, X.-K., Zheng, C., Wong, S. H.-S., & Ma, A. C.-H. (2022) · Aging · doi:10.18632/aging.204458 · Cited by 10 · see citing works
Lichterfeld, M., Cung, T., Seiss, K., Rosenberg, E. S., Pereyra, F., & Yu, X. G. (2012) · Journal of Virology · doi:10.1128/jvi.00196-12 · Cited by 9 · see citing works
- Authors
- Liu, Y., Sanoff, H. K., Cho, H., Burd, C. E., Torrice, C., Ibrahim, J. G., Thomas, N. E., & Sharpless, N. E.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Sharpless, Norman E.
- ORCID
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2009-07-21
- Volume
- 8
- Issue
- 4
- Pages
- 439-448
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC2752333
- OpenAlex
- W2038998835
- Cited by
- 509
- References
- 61
- Citations by year
- 2026: 41 · 2025: 25 · 2024: 63 · 2023: 39 · 2022: 40 · 2021: 45 · 2020: 44 · 2019: 24 · 2018: 32 · 2017: 19 · 2016: 24 · 2015: 17 · 2014: 20 · 2013: 23 · 2012: 17
- FWCI
- 11.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Aging Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- UNC Libraries
- Funders
- Burroughs Wellcome Fund
- Ellison Medical Foundation
- Wellcome Trust
- National Institutes of Health (5r01ag024379-15, ES014635, AG024379)
- National Institute on Aging (AG024379, R01-AG024379)
- National Cancer Institute (T32CA009156, R01CA112243, CA009156-34)
- National Institute of General Medical Sciences (R01GM070335)
- National Institute of Environmental Health Sciences (P01ES014635, ES014635, T32ES007126)
- National Center for Research Resources (RR023248, K12RR023248)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Social Sciences › Psychology › Neuropsychology and Physiological Psychology › Aging and Gerontology Research
- Keywords
- p16INK4a, aging biomarkers, peripheral blood T cells, tobacco use, physical inactivity, interleukin-6, frailty, tumor suppressor protein expression
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Aging, Female, Gene Expression Regulation, Humans, Male, Middle Aged, Smoking, T-Lymphocytes, Transcription, Genetic, Biomarkers, Exercise, Cyclin-Dependent Kinase Inhibitor p16, ADP-Ribosylation Factors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
