Identification of senescent cells in the bone microenvironment
Open accessAbstract
Cellular senescence is a fundamental mechanism by which cells remain metabolically active yet cease dividing and undergo distinct phenotypic alterations, including upregulation of p16Ink4a, profound secretome changes, telomere shortening, and decondensation of pericentromeric satellite DNA. Because senescent cells accumulate in multiple tissues with aging, these cells and the dysfunctional factors they secrete, termed the senescence-associated secretory phenotype (SASP), are increasingly recognized as promising therapeutic targets to prevent age-related degenerative pathologies, including osteoporosis. However, the cell type(s) within the bone microenvironment that undergoes senescence with aging in vivo has remained poorly understood, largely because previous studies have focused on senescence in cultured cells. Thus in young (age 6 months) and old (age 24 months) mice, we measured senescence and SASP markers in vivo in highly enriched cell populations, all rapidly isolated from bone/marrow without in vitro culture. In both females and males, p16Ink4a expression by real-time quantitative polymerase chain reaction (rt-qPCR) was significantly higher with aging in B cells, T cells, myeloid cells, osteoblast progenitors, osteoblasts, and osteocytes. Further, in vivo quantification of senescence-associated distension of satellites (SADS), ie, large-scale unraveling of pericentromeric satellite DNA, revealed significantly more senescent osteocytes in old compared with young bone cortices (11% versus 2%, p < 0.001). In addition, primary osteocytes from old mice had sixfold more (p < 0.001) telomere dysfunction-induced foci (TIFs) than osteocytes from young mice. Corresponding with the age-associated accumulation of senescent osteocytes was significantly higher expression of multiple SASP markers in osteocytes from old versus young mice, several of which also showed dramatic age-associated upregulation in myeloid cells. These data show that with aging, a subset of cells of various lineages within the bone microenvironment become senescent, although senescent myeloid cells and senescent osteocytes predominantly develop the SASP. Given the critical roles of osteocytes in orchestrating bone remodeling, our findings suggest that senescent osteocytes and their SASP may contribute to age-related bone loss. © 2016 American Society for Bone and Mineral Research
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The paper states that p16 is a key trigger of cellular senescence and has been proposed as a biomarker of mammalian aging.
“p16 is a key trigger of cellular senescence16, and its expression increases with aging in several rodent and primate tissues17–19, suggesting its potential use as a biomarker of mammalian aging.”
From Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial (2024) · cites this paper as [17]
The Introduction (page unavailable) calls p16Ink4a a principal effector of senescence and says its expression increases with age in several rodent and human tissues. The Results (page unavailable) call it a senescence biomarker and report higher expression in older mice and women. The paper does not describe p16 as a trigger of senescence or explicitly propose it as a biomarker of mammalian aging. (LLM, conf=0.82)
Experimental — accuracy not yet measuredLevels of DDR markers and TAFs increase during ageing in different mammalian tissues.
“Indeed, the levels of DDR markers and TAFs increase during ageing in different mammalian tissues.”
From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [35]
The Results (page unavailable) report substantially more telomere dysfunction-induced foci (TIFs) in osteocytes from old mice than in those from young mice, and higher p53 expression in some aged bone-cell populations. The paper does not establish that DDR markers and telomere-associated foci increase across different mammalian tissues; its findings are centered on the mouse bone microenvironment. (LLM, conf=0.84)
Experimental — accuracy not yet measuredMice, despite long telomeres and ubiquitous telomerase expression, show an age-dependent increase in dysfunctional telomeres in both proliferating and non-proliferating tissues.
“Mice, despite having long telomeres and ubiquitous telomerase expression, show an age-dependent increase in dysfunctional telomeres in both proliferating and non-proliferating tissues20,34–37.”
From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [35]
The Results report substantially more telomere dysfunction-induced foci in osteocytes from old mice than in those from young mice, supporting an age-related increase in this non-proliferating cell type. The paper does not establish the claimed increase across both proliferating and non-proliferating tissues, or state the premises about long mouse telomeres and ubiquitous telomerase expression. Page numbers were not available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn aged humans, needle biopsies of bone and bone marrow analysed by qPCR showed increased CDKN2A and CDKN1A, and SASP increased with age.
“Needle biopsies containing tissue of the bone and bone marrow analysed by qPCR revealed increased levels of CDKN2A and CDKN1A, and the SASP increased with age93.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [93]
The Results (page not provided) report that rt-qPCR of bone needle biopsies from older versus younger women found significantly higher p16Ink4a (CDKN2A) and p21 (CDKN1A) expression. Twelve SASP factors were also higher, but the 36-factor panel did not show a statistically significant increase as a group; the authors call the human SASP findings preliminary. The claim overstates that part as a general increase in the SASP. (LLM, conf=0.90)
Experimental — accuracy not yet measuredIn human bone biopsies, older women with mean age 78 years show upregulated mRNA expression of CDKN2A, CDKN1A and senescence-associated chemokines CCL2, CCL3, CCL8 and CSF1 compared with younger women.
“In human bone biopsies, older women (mean age 78 years) show upregulated mRNA expression of CDKN2A, CDKN1A and senescence-associated chemokines (for example, CCL2, CCL3, CCL8 and CSF1)93 compared with younger women.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [93]
Materials and Methods reports bone biopsies from older women with a mean age of 78 years, and Results reports higher p16Ink4a (CDKN2A) and p21 (CDKN1A) expression than in younger women. Results also reports 12 elevated SASP factors, but the passages do not identify CCL2, CCL3, CCL8 and CSF1 as elevated in the human biopsies; the paper calls those factor findings preliminary because the group-wide analysis was not statistically significant. Page numbers are unavailable in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measured
There is an accumulation of senescent B cells, T cells, myeloid cells, osteoprogenitors, osteoblasts, and osteocytes in bone biopsy samples from older, postmenopausal women compared to younger, premenopausal counterparts.
“These authors found that there is an accumulation of senescent B cells, T cells, myeloid cells, osteoprogenitors, osteoblasts, and osteocytes in bone biopsy samples from older, postmenopausal women compared to their younger, premenopausal counterparts, suggesting that these cells become senescent with age [37].”
From Osteoporosis: Molecular Pathology, Diagnostics, and Therapeutics (2023) · cites this paper as [37]
The Results report higher senescence-marker expression in bone biopsies from older than younger women. But the cell-by-cell findings for B cells, T cells, myeloid cells, osteoblast progenitors, osteoblasts, and osteocytes came from mice, not the women's biopsies. The paper gives the women's ages but does not identify their menopausal status. Page numbers are unavailable in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredγH2AX+ BMAds are substantially increased in both AD mice and old mice compared to their respective controls.
“Immunofluorescence using the DNA damage marker γH2AX, a robust marker of senescent cells50–52, also revealed a substantial increase in γH2AX+ BMAds in both AD mice (Fig. 3q,r) and old mice (Fig. 3s,t) compared with their respective controls.”
From Serum amyloid P secreted by bone marrow adipocytes drives skeletal amyloidosis (2025) · cites this paper as [52]
The citation is attached to the description of γH2AX as a senescence marker, not to the citing authors’ BMAd results. The Introduction describes persistent DNA damage as a feature of senescent cells, but our copy does not identify γH2AX as a robust marker. Its Results concern aging osteocytes, not γH2AX-positive BMAds in AD mice. (LLM, conf=0.80)
Experimental — accuracy not yet measuredSASP factor expression is significantly higher in osteocytes but not in osteoblast progenitors or osteoblasts.
“Expression of SASP factors, as measured by quantitative polymerase chain reaction (qPCR), is significantly increased in osteocytes but not in osteoblast progenitors or osteoblasts (45).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [45]
p21Cip1 is significantly increased mainly in osteocytes.
“p21Cip1 is significantly increased predominantly in osteocytes (45).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [45]
p16Ink4a is significantly higher in osteoprogenitors, osteoblasts, and osteocytes from old mice than in those from young mice.
“p16Ink4a is significantly increased in osteoprogenitors, osteoblasts, and osteocytes from old mice compared with those from young mice (45).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [45]
The same SASP factors are increased in bone marrow-derived myeloid cells but not in lymphocytes from old mice compared with young mice.
“The same SASP factors are upregulated in bone marrow–derived myeloid cells but not in lymphocytes from old mice relative to those from young mice (45).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [45]
Studies have identified oncogene-induced, irradiation-induced, and ageing-induced accumulation of senescent cells in bone marrow.
“Studies have identified oncogene-induced, irradiation-induced and ageing-induced accumulation of senescent cells in the bone marrow92–94.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [93]
Osteoblast progenitors and osteoblasts show a significant increase of Cdkn2a and a limited number of SASP factors.
“Osteoblast progenitors and osteoblasts exhibit a significant increase of Cdkn2a, in addition to an increase of a limited number of SASP factors93.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [93]
Osteocytes have increased SADS with age, plus increased Cdkn2a, Cdkn1a, Trp53 and numerous SASP transcripts.
“Osteocytes have increased SADS with age, in addition to an increase of Cdkn2a, Cdkn1a and Trp53 and numerous SASP transcripts93.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [93]
In aged mice, senescence markers are found in osteoblast progenitors, osteoblasts and osteocytes using magnetic-activated cell sorting followed by qPCR.
“In aged mice, markers of senescence have been found in osteoblast progenitors, osteoblasts and osteocytes using magnetic-activated cell sorting followed by qPCR.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [93]
In ageing and the listed disease states, skeletal cellular senescence can be observed through histological staining of SA-β-gal activity, SADS and TAF, typically in bone-embedded osteocytes.
“In both ageing and the disease states listed above, skeletal cellular senescence can also be observed through histological staining of SA-β-gal activity203, SADS93,200,204,205 and TAF200,203,204, typically in bone-embedded osteocytes206.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [93]
Osteoblasts are among the major cell types known to undergo cellular senescence during aging.
“Osteoblasts are among the major cell types known to undergo cellular senescence during aging52,60.”
From Serum amyloid P secreted by bone marrow adipocytes drives skeletal amyloidosis (2025) · cites this paper as [52]
In various murine liver injury models, stellate cells can acquire senescence markers including p21, p16, and SA-β-gal, and express certain SASP factors.
“In various murine liver injury models, stellate cells can acquire senescence markers, including p21, p16, and SA-β-gal, and express certain SASP factors80–83.”
From Guidelines for minimal information on cellular senescence experimentation in vivo (2024) · cites this paper as [81]
The Discussion mentions senescence markers in hepatocytes, while the Results report p21, p16 and SASP factors in aging bone cells. Neither section addresses stellate cells in murine liver injury models; searches for stellate cells and liver injury found no passage supporting that specific claim. No page numbers were available in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredDuring aging, as well as under the action of several stressors, senescent osteocytes accumulate in the bone microenvironment and acquire a distinctive proinflammatory secretome, termed the senescence-associated secretory phenotype (SASP), which leads to imbalanced bone remodeling with increased resorption and decreased formation.
“In fact, during aging, as well as under the action of several stressors [see Farr et al.91 for a review], senescent osteocytes accumulate in the bone microenvironment and acquire a distinctive proinflammatory secretome, termed the senescence-associated secretory phenotype (SASP),92 which leads to imbalanced bone remodeling with increased resorption and decreased formation.”
From Bone remodeling: an operational process ensuring survival and bone mechanical competence (2022) · cites this paper as [92]
Senotherapeutic drugs could potentially treat a variety of conditions primarily or secondarily mediated by senescent cell accumulation.
“The use of senotherapeutic drugs could potentially be effective in treating a variety of conditions primarily or secondarily mediated by accumulation of senescent cells [6, 33, 67–87].”
From Reducing Senescent Cell Burden in Aging and Disease (2020) · cites this paper as [70]
Cardiomyocytes, osteocytes, osteoblasts, adipocytes, neurons, and retinal ganglion cells are post-mitotic cell types that have been shown to possess a senescence-like phenotype in mice.
“Cardiomyocytes, osteocytes, osteoblasts, adipocytes, neurons, and retinal ganglion cells are all post-mitotic cell types that have been shown to possess a senescence-like phenotype in mice”
From Skeletal muscle aging, cellular senescence, and senotherapeutics: current knowledge and future directions (2021) · cites this paper as Farr et al., 2016
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Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625 · see citing works
LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing.
Kabeya, Y., Mizushima, N., Ueno, T., Yamamoto, A., Kirisako, T., Noda, T., Kominami, E., Ohsumi, Y., & Yoshimori, T. (2000) · The EMBO Journal · doi:10.1093/emboj/19.21.5720 · Cited by 6,605 · see citing works
Cui, C., Cui, J., Jin, F., Cui, Y., Li, R., Jiang, X., Tian, Y., Wang, R. C., Jiang, P., & Gao, J. (2017) · Cellular Physiology and Biochemistry · doi:10.1159/000479571 · Cited by 5,214 · see citing works
The senescence-associated secretory phenotype: the dark side of tumor suppression
Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-121808-102144 · Cited by 5,206 · see citing works
Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders
Baker, D. J., Wijshake, T., Tchkonia, T., LeBrasseur, N. K., Childs, B. G., van de Sluis, B., Kirkland, J. L., & van Deursen, J. M. (2011) · Nature · doi:10.1038/nature10600 · Cited by 3,670 · cited 5× · see citing works
“related pathologies in non-skeletal tissues, (14,15) in combination with our data, it seems reasonable to hypothesize that accumulation of senescent cells in the bone microenvironment, particularly those that develop the SASP, is one potential mechanism driving age-related bone loss.”
InfluentialSelf-citationNaturally 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
The role of senescent cells in ageing
van Deursen, J. M. (2014) · Nature · doi:10.1038/nature13193 · Cited by 2,623 · see citing works
The Achilles' heel of senescent cells: from transcriptome to senolytic drugs
Zhu, Y., Tchkonia, T., Pirtskhalava, T., Gower, A. C., Ding, H., Giorgadze, N., Palmer, A. K., Ikeno, Y., Hubbard, G. B., Lenburg, M., et al. (2015) · Aging Cell · doi:10.1111/acel.12344 · Cited by 2,562 · see citing works
Self-citationCellular senescence in aging and age-related disease: from mechanisms to therapy
Childs, B. G., Durik, M., Baker, D. J., & van Deursen, J. M. (2015) · Nature Medicine · doi:10.1038/nm.4000 · Cited by 2,363 · see citing works
Impairment of starvation-induced and constitutive autophagy in <i>Atg7</i> -deficient mice
Komatsu, M., Waguri, S., Ueno, T., Iwata, J., Murata, S., Tanida, I., Ezaki, J., Mizushima, N., Ohsumi, Y., Uchiyama, Y., et al. (2005) · The Journal of Cell Biology · doi:10.1083/jcb.200412022 · Cited by 2,331 · see citing works
A complex secretory program orchestrated by the inflammasome controls paracrine senescence
Acosta, J. C., Banito, A., Wuestefeld, T., Georgilis, A., Janich, P., Morton, J. P., Athineos, D., Kang, T.-W., Lasitschka, F., Andrulis, M., et al. (2013) · Nature Cell Biology · doi:10.1038/ncb2784 · Cited by 2,278 · see citing works
Evidence for osteocyte regulation of bone homeostasis through RANKL expression
Nakashima, T., Hayashi, M., Fukunaga, T., Kurata, K., Oh-hora, M., Feng, J. Q., Bonewald, L. F., Kodama, T., Wutz, A., Wagner, E. F., et al. (2011) · Nature Medicine · doi:10.1038/nm.2452 · Cited by 1,778 · see citing works
Self-citationCellular senescence and the senescent secretory phenotype: therapeutic opportunities
Tchkonia, T., Zhu, Y., van Deursen, J., Campisi, J., & Kirkland, J. L. (2013) · Journal of Clinical Investigation · doi:10.1172/jci64098 · Cited by 1,774 · see citing works
Self-citationInk4a/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
Reversal of human cellular senescence: roles of the p53 and p16 pathways
Beauséjour, C. M., Krtolica, A., Galimi, F., Narita, M., Lowe, S. W., Yaswen, P., & Campisi, J. (2003) · The EMBO Journal · doi:10.1093/emboj/cdg417 · Cited by 1,457 · see citing works
Zhou, B. O., Yue, R., Murphy, M. M., Peyer, J. G., & Morrison, S. J. (2014) · Cell Stem Cell · doi:10.1016/j.stem.2014.06.008 · Cited by 1,381 · see citing works
Autophagy maintains stemness by preventing senescence
García-Prat, L., Martínez-Vicente, M., Perdiguero, E., Ortet, L., Rodríguez-Ubreva, J., Rebollo, E., Ruiz-Bonilla, V., Gutarra, S., Ballestar, E., Serrano, A. L., et al. (2016) · Nature · doi:10.1038/nature16187 · Cited by 1,355 · see citing works
Matrix-embedded cells control osteoclast formation
Xiong, J., Onal, M., Jilka, R. L., Weinstein, R. S., Manolagas, S. C., & O'Brien, C. A. (2011) · Nature Medicine · doi:10.1038/nm.2448 · Cited by 1,304 · see citing works
Cellular 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 Osteocyte: An Endocrine Cell … and More
Dallas, S. L., Prideaux, M., & Bonewald, L. F. (2013) · Endocrine Reviews · doi:10.1210/er.2012-1026 · Cited by 1,042 · see citing works
Self-citationThe DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4.
Kang, C., Xu, Q., Martin, T. D., Li, M. Z., Demaria, M., Aron, L., Lu, T., Yankner, B. A., Campisi, J., & Elledge, S. J. (2015) · Science · doi:10.1126/science.aaa5612 · Cited by 982 · see citing works
A crucial role for adipose tissue p53 in the regulation of insulin resistance
Minamino, T., Orimo, M., Shimizu, I., Kunieda, T., Yokoyama, M., Ito, T., Nojima, A., Nabetani, A., Oike, Y., Matsubara, H., et al. (2009) · Nature Medicine · doi:10.1038/nm.2014 · Cited by 891 · see citing works
Chronic inflammation induces telomere dysfunction and accelerates ageing in mice
Jurk, D., Wilson, C., Passos, J. F., Oakley, F., Correia-Melo, C., Greaves, L., Saretzki, G., Fox, C., Lawless, C., Anderson, R., et al. (2014) · Nature Communications · doi:10.1038/ncomms5172 · Cited by 814 · see citing works
On testing the significance of sets of genes
Efron, B., & Tibshirani, R. J. (2007) · The Annals of Applied Statistics · doi:10.1214/07-aoas101 · Cited by 785 · see citing works
Salminen, A., Kauppinen, A., & Kaarniranta, K. (2012) · Cellular Signalling · doi:10.1016/j.cellsig.2011.12.006 · Cited by 763 · see citing works
A senescent cell bystander effect: senescence‐induced senescence
Nelson, G., Wordsworth, J., Wang, C., Jurk, D., Lawless, C., Martin‐Ruiz, C., & von Zglinicki, T. (2012) · Aging Cell · doi:10.1111/j.1474-9726.2012.00795.x · Cited by 755 · see citing works
Jurk, D., Wang, C., Miwa, S., Maddick, M., Korolchuk, V., Tsolou, A., Gonos, E. S., Thrasivoulou, C., Jill Saffrey, M., Cameron, K., et al. (2012) · Aging Cell · doi:10.1111/j.1474-9726.2012.00870.x · Cited by 598 · see citing works
(1995) · PubMed · Cited by 496 · see citing works
Demonstration of osteocytic perilacunar/canalicular remodeling in mice during lactation
Qing, H., Ardeshirpour, L., Divieti Pajevic, P., Dusevich, V., Jähn, K., Kato, S., Wysolmerski, J., & Bonewald, L. F. (2012) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.1567 · Cited by 489 · see citing works
Self-citationMonitoring 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
Human cell senescence as a DNA damage response
Zglinicki, T. V., Saretzki, G., Ladhoff, J., Fagagna, F. D. D., & Jackson, S. P. (2005) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2004.09.034 · Cited by 419 · see citing works
Mitochondrial effectors of cellular senescence: beyond the free radical theory of aging
Ziegler, D. V., Wiley, C. D., & Velarde, M. C. (2014) · Aging Cell · doi:10.1111/acel.12287 · Cited by 353 · see citing works
DMP1-targeted Cre Expression in Odontoblasts and Osteocytes
Lu, Y., Xie, Y., Zhang, S., Dusevich, V., Bonewald, L. F., & Feng, J. Q. (2007) · Journal of Dental Research · doi:10.1177/154405910708600404 · Cited by 350 · see citing works
Self-citationGoldman, D. P., Cutler, D., Rowe, J. W., Michaud, P., Sullivan, J. H., Peneva, D., & Olshansky, S. J. (2013) · Health Affairs · doi:10.1377/hlthaff.2013.0052 · Cited by 312 · 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 · 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
Identification of differentially expressed genes between osteoblasts and osteocytes
Paić, F., Igwe, J. C., Nori, R., Kronenberg, M. S., Franceschetti, T., Harrington, P., Kuo, L., Shin, D., Rowe, D. W., Harris, S. E., et al. (2009) · Bone · doi:10.1016/j.bone.2009.06.010 · Cited by 261 · see citing works
Swanson, E. C., Manning, B., Zhang, H., & Lawrence, J. B. (2013) · Journal of Cell Biology · doi:10.1083/jcb.201306073 · Cited by 251 · cited 2× · see citing works
“Recent work has shown that pericentromeric satellite heterochromatin undergoes decondensation in cell senescence, and that this large-scale unraveling of pericentromeric satellite DNA, termed SADS, is a robust marker of cell senescence in vivo.((5)) Detailed procedures for the SADS assay are described in the Supplemen…”
Senescence‐associated intrinsic mechanisms of osteoblast dysfunctions
Kassem, M., & Marie, P. (2011) · Aging Cell · doi:10.1111/j.1474-9726.2011.00669.x · Cited by 228 · see citing works
Isolation and Culture of Primary Osteocytes from the Long Bones of Skeletally Mature and Aged Mice
Stern, A. R., Stern, M. M., Dyke, M. E. V., Jähn, K., Prideaux, M., & Bonewald, L. F. (2012) · BioTechniques · doi:10.2144/0000113876 · Cited by 207 · see citing works
Self-citationSuppression of Autophagy in Osteocytes Mimics Skeletal Aging
Onal, M., Piemontese, M., Xiong, J., Wang, Y., Han, L., Ye, S., Komatsu, M., Selig, M., Weinstein, R. S., Zhao, H., et al. (2013) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.444190 · Cited by 206 · see citing works
The role of DNA damage repair in aging of adult stem cells
Kenyon, J. D., & Gerson, S. L. (2007) · Nucleic Acids Research · doi:10.1093/nar/gkm1064 · Cited by 152 · see citing works
DNA damage drives accelerated bone aging via an NF- <b>κ</b> B–dependent mechanism
Chen, Q., Liu, K., Robinson, A. R., Clauson, C. L., Blair, H. C., Robbins, P. D., Niedernhofer, L. J., & Ouyang, H. (2013) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.1851 · Cited by 135 · see citing works
p21 Both Attenuates and Drives Senescence and Aging in BubR1 Progeroid Mice
Baker, D. J., Weaver, R. L., & van Deursen, J. M. (2013) · Cell Reports · doi:10.1016/j.celrep.2013.03.028 · Cited by 130 · see citing works
Bone Cell Senescence: Mechanisms and Perspectives
Marie, P. J. (2014) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.2190 · Cited by 82 · see citing works
Nioi, P., Taylor, S., Hu, R., Pacheco, E., He, Y. D., Hamadeh, H. K., Pászty, C., Pyrah, I. T. G., Ominsky, M. S., & Boyce, R. W. (2015) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.2482 · Cited by 75 · see citing works
Effects of Age and Estrogen on Skeletal Gene Expression in Humans as Assessed by RNA Sequencing
Farr, J. N., Roforth, M. M., Fujita, K., Nicks, K. M., Cunningham, J. M., Atkinson, E. J., Therneau, T. M., McCready, L. K., Peterson, J. M., Drake, M. T., et al. (2015) · PLOS ONE · doi:10.1371/journal.pone.0138347 · Cited by 75 · see citing works
Self-citationEffects of chronic estrogen treatment on modulating age-related bone loss in female mice
Syed, F. A., Mödder, U. I., Roforth, M. M., Hensen, I., Fraser, D. G., Peterson, J. M., Oursler, M. J., & Khosla, S. (2010) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.129 · Cited by 52 · see citing works
Self-citationIsolation and characterization of human osteoblasts from needle biopsies without in vitro culture
Fujita, K., Roforth, M. M., Atkinson, E. J., Peterson, J. M., Drake, M. T., McCready, L. K., Farr, J. N., Monroe, D. G., & Khosla, S. (2013) · Osteoporosis International · doi:10.1007/s00198-013-2529-9 · Cited by 29 · see citing works
Self-citationA novel purification method for multipotential skeletal stem cells
Itoh, S., & Aubin, J. E. (2009) · Journal of Cellular Biochemistry · doi:10.1002/jcb.22262 · Cited by 27 · see citing works
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Sorted by citations
Senolytics improve physical function and increase lifespan in old age
Xu, M., Pirtskhalava, T., Farr, J. N., Weigand, B. M., Palmer, A. K., Weivoda, M. M., Inman, C. L., Ogrodnik, M. B., Hachfeld, C. M., Fraser, D. G., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0092-9 · Cited by 2,287 · see citing works
Self-citationHickson, L. J., Langhi Prata, L. G. P., Bobart, S. A., Evans, T. K., Giorgadze, N., Hashmi, S. K., Herrmann, S. M., Jensen, M. D., Jia, Q., Jordan, K. L., et al. (2019) · EBioMedicine · doi:10.1016/j.ebiom.2019.08.069 · Cited by 1,383 · 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
Senolytic drugs: from discovery to translation
Kirkland, J. L., & Tchkonia, T. (2020) · Journal of Internal Medicine · doi:10.1111/joim.13141 · Cited by 1,227 · see citing works
Self-citationTargeting cellular senescence prevents age-related bone loss in mice
Farr, J. N., Xu, M., Weivoda, M. M., Monroe, D. G., Fraser, D. G., Onken, J. L., Negley, B. A., Sfeir, J. G., Ogrodnik, M. B., Hachfeld, C. M., et al. (2017) · Nature Medicine · doi:10.1038/nm.4385 · Cited by 1,182 · see citing works
Self-citationCellular senescence and senolytics: the path to the clinic
Chaib, S., Tchkonia, T., & Kirkland, J. L. (2022) · Nature Medicine · doi:10.1038/s41591-022-01923-y · Cited by 1,105 · see citing works
Self-citationA new gene set identifies senescent cells and predicts senescence-associated pathways across tissues
Saul, D., Kosinsky, R. L., Atkinson, E. J., Doolittle, M. L., Zhang, X., LeBrasseur, N. K., Pignolo, R. J., Robbins, P. D., Niedernhofer, L. J., Ikeno, Y., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-32552-1 · Cited by 1,060 · see citing works
Self-citationMechanisms and therapeutic implications of cellular senescence in osteoarthritis
Coryell, P. R., Diekman, B. O., & Loeser, R. F. (2021) · Nature Reviews Rheumatology · doi:10.1038/s41584-020-00533-7 · Cited by 761 · see citing works
Telomere dysfunction in ageing and age-related diseases
Rossiello, F., Jurk, D., Passos, J. F., & d’Adda di Fagagna, F. (2022) · Nature Cell Biology · doi:10.1038/s41556-022-00842-x · Cited by 754 · see citing works
The role of cellular senescence in ageing and endocrine disease
Khosla, S., Farr, J. N., Tchkonia, T., & Kirkland, J. L. (2020) · Nature Reviews Endocrinology · doi:10.1038/s41574-020-0335-y · Cited by 523 · see citing works
Self-citationRobling, A. G., & Bonewald, L. F. (2020) · Annual Review of Physiology · doi:10.1146/annurev-physiol-021119-034332 · Cited by 539 · see citing works
Senescent cell clearance by the immune system: Emerging therapeutic opportunities
Prata, L. G. P. L., Ovsyannikova, I. G., Tchkonia, T., & Kirkland, J. L. (2018) · Seminars in Immunology · doi:10.1016/j.smim.2019.04.003 · Cited by 497 · see citing works
Self-citationMolecular mechanosensors in osteocytes
Qin, L., Liu, W., Cao, H., & Xiao, G. (2020) · Bone Research · doi:10.1038/s41413-020-0099-y · Cited by 484 · see citing works
Bone remodeling: an operational process ensuring survival and bone mechanical competence
Bolamperti, S., Villa, I., & Rubinacci, A. (2022) · Bone Research · doi:10.1038/s41413-022-00219-8 · Cited by 482 · see citing works
Advances in pathogenesis and therapeutic strategies for osteoporosis
Song, S., Guo, Y., Yang, Y., & Fu, D. (2022) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2022.108168 · Cited by 476 · see citing works
Mitochondria in Cell Senescence: Is Mitophagy the Weakest Link?
Korolchuk, V. I., Miwa, S., Carroll, B., & von Zglinicki, T. (2017) · EBioMedicine · doi:10.1016/j.ebiom.2017.03.020 · Cited by 409 · see citing works
“, 2016), osteocytes (Farr et al., 2016)) proliferation rates as well as in postmitotic tissues (neurons (Jurk et al.”
BackgroundSenNet 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
Self-citationCellular senescence in osteoarthritis pathology
McCulloch, K., Litherland, G. J., & Rai, T. S. (2017) · Aging Cell · doi:10.1111/acel.12562 · Cited by 367 · 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
Self-citationOgrodnik, M. (2021) · Aging Cell · doi:10.1111/acel.13338 · Cited by 349 · see citing works
Self-citationSenolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span
Robbins, P. D., Jurk, D., Khosla, S., Kirkland, J. L., LeBrasseur, N. K., Miller, J. D., Passos, J. F., Pignolo, R. J., Tchkonia, T., & Niedernhofer, L. J. (2021) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev-pharmtox-050120-105018 · Cited by 339 · see citing works
“Expression of SASP factors, as measured by quantitative polymerase chain reaction (qPCR), is significantly increased in osteocytes but not in osteoblast progenitors or osteoblasts (45).”
BackgroundInfluentialSelf-citationStress, cell senescence and organismal ageing
de Magalhães, J. P., & Passos, J. F. (2018) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2017.07.001 · Cited by 316 · see citing works
A Senescence-Centric View of Aging: Implications for Longevity and Disease
Borghesan, M., Hoogaars, W. M. H., Varela-Eirin, M., Talma, N., & Demaria, M. (2020) · Trends in Cell Biology · doi:10.1016/j.tcb.2020.07.002 · Cited by 267 · see citing works
Farr, J. N., & Khosla, S. (2019) · Bone · doi:10.1016/j.bone.2019.01.015 · Cited by 263 · see citing works
Self-citationCellular senescence and Alzheimer disease: the egg and the chicken scenario
Saez-Atienzar, S., & Masliah, E. (2020) · Nature Reviews Neuroscience · doi:10.1038/s41583-020-0325-z · Cited by 257 · see citing works
Tuttle, C. S. L., Waaijer, M. E. C., Slee‐Valentijn, M. S., Stijnen, T., Westendorp, R., & Maier, A. B. (2020) · Aging Cell · doi:10.1111/acel.13083 · Cited by 211 · see citing works
Herdy, J. R., Traxler, L., Agarwal, R. K., Karbacher, L., Schlachetzki, J. C. M., Boehnke, L., Zangwill, D., Galasko, D., Glass, C. K., Mertens, J., et al. (2022) · Cell Stem Cell · doi:10.1016/j.stem.2022.11.010 · Cited by 208 · see citing works
Cellular Senescence in Postmitotic Cells: Beyond Growth Arrest
Sapieha, P., & Mallette, F. A. (2018) · Trends in Cell Biology · doi:10.1016/j.tcb.2018.03.003 · Cited by 193 · see citing works
Kim, H., Chang, J., Shao, L., Han, L., Iyer, S., Manolagas, S. C., O'Brien, C. A., Jilka, R. L., Zhou, D., & Almeida, M. (2017) · Aging Cell · doi:10.1111/acel.12597 · Cited by 192 · see citing works
Reducing Senescent Cell Burden in Aging and Disease
Pignolo, R. J., Passos, J. F., Khosla, S., Tchkonia, T., & Kirkland, J. L. (2020) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2020.03.005 · Cited by 177 · see citing works
Self-citationFracture Healing in the Setting of Endocrine Diseases, Aging, and Cellular Senescence
Saul, D., & Khosla, S. (2022) · Endocrine Reviews · doi:10.1210/endrev/bnac008 · Cited by 185 · see citing works
Self-citationSenescence in Post-Mitotic Cells: A Driver of Aging?
von Zglinicki, T., Wan, T., & Miwa, S. (2021) · Antioxidants & Redox Signaling · doi:10.1089/ars.2020.8048 · Cited by 170 · 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
Osteoporosis: Molecular Pathology, Diagnostics, and Therapeutics
Adejuyigbe, B., Kallini, J., Chiou, D., & Kallini, J. R. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241914583 · Cited by 148 · see citing works
Targeted Reduction of Senescent Cell Burden Alleviates Focal Radiotherapy-Related Bone Loss
Chandra, A., Lagnado, A. B., Farr, J. N., Monroe, D. G., Park, S., Hachfeld, C., Tchkonia, T., Kirkland, J. L., Khosla, S., Passos, J. F., et al. (2020) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.3978 · Cited by 138 · see citing works
Self-citationAccelerated osteocyte senescence and skeletal fragility in mice with type 2 diabetes
Eckhardt, B. A., Rowsey, J. L., Thicke, B. S., Fraser, D. G., O’Grady, K. L., Bondar, O. P., Hines, J. M., Singh, R. J., Thoreson, A. R., Rakshit, K., et al. (2020) · JCI Insight · doi:10.1172/jci.insight.135236 · Cited by 130 · see citing works
Self-citationInhibiting Cellular Senescence: A New Therapeutic Paradigm for Age-Related Osteoporosis
Khosla, S., Farr, J. N., & Kirkland, J. L. (2018) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2017-02694 · Cited by 130 · see citing works
Self-citationTchkonia, T., Palmer, A. K., & Kirkland, J. L. (2021) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgaa728 · Cited by 129 · see citing works
Self-citationSympathetic β1-adrenergic signaling contributes to regulation of human bone metabolism
Khosla, S., Drake, M. T., Volkman, T. L., Thicke, B. S., Achenbach, S. J., Atkinson, E. J., Joyner, M. J., Rosen, C. J., Monroe, D. G., & Farr, J. N. (2018) · Journal of Clinical Investigation · doi:10.1172/jci122151 · Cited by 132 · see citing works
Self-citationSharma, A. K., Roberts, R. L., Benson, R. D., Pierce, J. L., Yu, K., Hamrick, M. W., & McGee-Lawrence, M. E. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.00354 · Cited by 131 · see citing works
Ali, D., Tencerova, M., Figeac, F., Kassem, M., & Jafari, A. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.981487 · Cited by 122 · see citing works
“Analysis of human bone s p e c im en s h a d s h own p r e s e n c e o f s e n e s c e n c e microenvironment in the bone tissue obtained from old individuals compared to young control subjects, evidenced by increased expression of p16 and p21 (31).”
BackgroundFarr, 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
“p16 is a key trigger of cellular senescence 16 , and its expression increases with aging in several rodent and primate tissues 17–19 , suggesting its potential use as a biomarker of mammalian aging.”
Self-citationChandra, A., Lagnado, A. B., Farr, J. N., Doolittle, M., Tchkonia, T., Kirkland, J. L., LeBrasseur, N. K., Robbins, P. D., Niedernhofer, L. J., Ikeno, Y., et al. (2022) · Aging Cell · doi:10.1111/acel.13602 · Cited by 120 · see citing works
Self-citationCellular senescence in aging and age-related diseases: Implications for neurodegenerative diseases
(2020) · International Review of Neurobiology · doi:10.1016/bs.irn.2020.03.019 · Cited by 114 · see citing works
Self-citationAquino-Martinez, R., Rowsey, J. L., Fraser, D. G., Eckhardt, B. A., Khosla, S., Farr, J. N., & Monroe, D. G. (2020) · Bone · doi:10.1016/j.bone.2019.115220 · Cited by 114 · see citing works
“For fluorescent in situ hybridization (FISH) staining, bone sections were processed as previously described [23].”
BackgroundMethodInfluentialSelf-citationAge-associated callus senescent cells produce TGF-β1 that inhibits fracture healing in aged mice
Liu, J., Zhang, J., Lin, X., Boyce, B. F., Zhang, H., & Xing, L. (2022) · Journal of Clinical Investigation · doi:10.1172/jci148073 · Cited by 112 · see citing works
Expansion and Cell-Cycle Arrest: Common Denominators of Cellular Senescence
Ogrodnik, M., Salmonowicz, H., Jurk, D., & Passos, J. F. (2019) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2019.06.011 · Cited by 104 · see citing works
Self-citationEnglund, 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
Self-citationp21 induces a senescence program and skeletal muscle dysfunction
Englund, D. A., Jolliffe, A., Aversa, Z., Zhang, X., Sturmlechner, I., Sakamoto, A. E., Zeidler, J. D., Warner, G. M., McNinch, C., White, T. A., et al. (2023) · Molecular Metabolism · doi:10.1016/j.molmet.2022.101652 · Cited by 90 · see citing works
Self-citationMusculoskeletal senescence: a moving target ready to be eliminated
Baar, M. P., Perdiguero, E., Muñoz-Cánoves, P., & de Keizer, P. L. (2018) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2018.05.007 · Cited by 83 · see citing works
Local senolysis in aged mice only partially replicates the benefits of systemic senolysis
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Self-citationMitochondria and cellular senescence: Implications for musculoskeletal ageing
Habiballa, L., Salmonowicz, H., & Passos, J. F. (2019) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.10.417 · Cited by 82 · see citing works
Aquino‐Martinez, R., Eckhardt, B. A., Rowsey, J. L., Fraser, D. G., Khosla, S., Farr, J. N., & Monroe, D. G. (2021) · Journal of Periodontology · doi:10.1002/jper.20-0529 · Cited by 78 · see citing works
Self-citationTargeting senescent cells improves functional recovery after spinal cord injury
Paramos-de-Carvalho, D., Martins, I., Cristóvão, A. M., Dias, A. F., Neves-Silva, D., Pereira, T., Chapela, D., Farinho, A., Jacinto, A., & Saúde, L. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.109334 · Cited by 74 · see citing works
Modulation of fracture healing by the transient accumulation of senescent cells
Saul, D., Monroe, D. G., Rowsey, J. L., Kosinsky, R. L., Vos, S. J., Doolittle, M. L., Farr, J. N., & Khosla, S. (2021) · eLife · doi:10.7554/elife.69958 · Cited by 71 · see citing works
Self-citationBai, J., Wang, Y., Wang, J., Zhai, J., He, F., & Zhu, G. (2020) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00520.2019 · Cited by 72 · see citing works
Yang, R., Zhang, J., Li, J., Qin, R., Chen, J., Wang, R., Goltzman, D., & Miao, D. (2022) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2021.12.010 · Cited by 67 · see citing works
Farr, J. N., Kaur, J., Doolittle, M. L., & Khosla, S. (2020) · Current Osteoporosis Reports · doi:10.1007/s11914-020-00619-x · Cited by 60 · see citing works
Self-citationDoolittle, M. L., Saul, D., Kaur, J., Rowsey, J. L., Vos, S. J., Pavelko, K. D., Farr, J. N., Monroe, D. G., & Khosla, S. (2023) · Nature Communications · doi:10.1038/s41467-023-40393-9 · Cited by 57 · see citing works
Self-citationDoolittle, M. L., Saul, D., Kaur, J., Rowsey, J. L., Vos, S. J., Pavelko, K. D., Farr, J. N., Monroe, D. G., & Khosla, S. (2023) · doi:10.1101/2023.01.12.523760 · Cited by 57 · see citing works
Self-citationRoadmap for alleviating the manifestations of ageing in the cardiovascular system
Liberale, L., Tual-Chalot, S., Sedej, S., Ministrini, S., Georgiopoulos, G., Grunewald, M., Bäck, M., Bochaton-Piallat, M.-L., Boon, R. A., Ramos, G. C., et al. (2025) · Nature Reviews Cardiology · doi:10.1038/s41569-025-01130-5 · Cited by 59 · see citing works
Self-citationThe Senolytic Drug Fisetin Attenuates Bone Degeneration in the Zmpste24−/− Progeria Mouse Model
Hambright, W. S., Mu, X., Gao, X., Guo, P., Kawakami, Y., Mitchell, J., Mullen, M., Nelson, A.-L., Bahney, C., Nishimura, H., et al. (2023) · Journal of Osteoporosis · doi:10.1155/2023/5572754 · Cited by 44 · see citing works
Samakkarnthai, P., Saul, D., Zhang, L., Aversa, Z., Doolittle, M. L., Sfeir, J. G., Kaur, J., Atkinson, E. J., Edwards, J. R., Russell, G. G., et al. (2023) · Aging · doi:10.18632/aging.204701 · Cited by 34 · see citing works
Self-citationYamada, C., Ho, A., Akkaoui, J., Garcia, C., Duarte, C., & Movila, A. (2021) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2021.111503 · Cited by 33 · see citing works
Context‐dependent roles of cellular senescence in normal, aged, and disease states
Moiseeva, V., Cisneros, A., Cobos, A. C., Tarrega, A. B., Oñate, C. S., Perdiguero, E., Serrano, A. L., & Muñoz‐Cánoves, P. (2023) · The FEBS Journal · doi:10.1111/febs.16573 · Cited by 34 · see citing works
Xu, J.-Z., Zhou, Y.-M., Zhang, L.-L., Chen, X.-J., Yang, Y.-Y., Zhang, D., Zhu, K.-C., Kong, X.-K., Sun, L.-H., Tao, B., et al. (2022) · Cell Death Discovery · doi:10.1038/s41420-022-01048-8 · Cited by 22 · see citing works
Serum amyloid P secreted by bone marrow adipocytes drives skeletal amyloidosis
Kumar, S., Song, K., Wang, J., Baghel, M. S., Zeng, Y., Shen, K., Zheng, J., Crane, J., Demehri, S., Gao, P., et al. (2025) · Nature Aging · doi:10.1038/s43587-025-00924-z · Cited by 16 · see citing works
Overview of molecular signatures of senescence and associated resources: pros and cons
Ntintas, O. A., Vagena, S., Pantelis, P., Theocharous, G., Petty, R., Evangelou, K., & Gorgoulis, V. G. (2026) · FEBS Open Bio · doi:10.1002/2211-5463.70134 · Cited by 6 · see citing works
- Authors
- Farr, J. N., Fraser, D. G., Wang, H., Jaehn, K., Ogrodnik, M. B., Weivoda, M. M., Drake, M. T., Tchkonia, T., LeBrasseur, N. K., Kirkland, J. L., Bonewald, L. F., Pignolo, R. J., Monroe, D. G., & Khosla, S.
- Affiliations
- Mayo Clinic (US)
- University of Pennsylvania (US)
- Department of Oral BiologyUniversity of Missouri-Kansas City, School of DentistryKansas CityMOUSA
- Robert and Arlene Kogod Center on Aging and Endocrine Research UnitMayo Clinic College of MedicineRochesterMNUSA
- University of Missouri–Kansas City (US)
- Corresponding author
- Farr, Joshua N
- Khosla, Sundeep
- ORCID
- Venue
- Journal of Bone and Mineral Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-06-24
- Volume
- 31
- Issue
- 11
- Pages
- 1920-1929
- ISSN
- 0884-0431 (ISSN-L)
- 1523-4681
- PMC
- PMC5289710
- OpenAlex
- W2467271588
- Semantic Scholar
- 9187e3c8c3d813a208378f001457959a3a0b1829
- Cited by
- 562
- References
- 50
- Citations by year
- 2026: 56 · 2025: 77 · 2024: 79 · 2023: 77 · 2022: 64 · 2021: 61 · 2020: 61 · 2019: 39 · 2018: 28 · 2017: 17 · 2016: 2
- FWCI
- 22.89
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Journal of Bone and Mineral Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Newcastle University
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Keywords
- cellular senescence, senescence-associated secretory phenotype, bone microenvironment, osteocytes, osteoblasts, myeloid cells, p16INK4a, telomere dysfunction, bone aging, osteoporosis, age-related bone loss
- MeSH terms
- Animals, Bone and Bones, Cells, Cultured, DNA, Satellite, Female, Male, Mice, Inbred C57BL, Osteoblasts, Osteocytes, Phenotype, Biomarkers, Cellular Senescence, Cell Lineage, Cyclin-Dependent Kinase Inhibitor p16, Myeloid Cells, Cellular Microenvironment
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