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Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial
Open accessAbstract
Preclinical evidence demonstrates that senescent cells accumulate with aging and that senolytics delay multiple age-related morbidities, including bone loss. Thus, we conducted a phase 2 randomized controlled trial of intermittent administration of the senolytic combination dasatinib plus quercetin (D + Q) in postmenopausal women (n = 60 participants). The primary endpoint, percentage changes at 20 weeks in the bone resorption marker C-terminal telopeptide of type 1 collagen (CTx), did not differ between groups (median (interquartile range), D + Q -4.1% (-13.2, 2.6), control -7.7% (-20.1, 14.3); P = 0.611). The secondary endpoint, percentage changes in the bone formation marker procollagen type 1 N-terminal propeptide (P1NP), increased significantly (relative to control) in the D + Q group at both 2 weeks (+16%, P = 0.020) and 4 weeks (+16%, P = 0.024), but was not different from control at 20 weeks (-9%, P = 0.149). No serious adverse events were observed. In exploratory analyses, the skeletal response to D + Q was driven principally by women with a high senescent cell burden (highest tertile for T cell p16 (also known as CDKN2A) mRNA levels) in which D + Q concomitantly increased P1NP (+34%, P = 0.035) and reduced CTx (-11%, P = 0.049) at 2 weeks, and increased radius bone mineral density (+2.7%, P = 0.004) at 20 weeks. Thus, intermittent D + Q treatment did not reduce bone resorption in the overall group of postmenopausal women. However, our exploratory analyses indicate that further studies are needed testing the hypothesis that the underlying senescent cell burden may dictate the clinical response to senolytics. ClinicalTrials.gov identifier: NCT04313634 .
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“serum P1NP increased at 2 weeks in the T3 D + Q group (relative to control, +34%, P = 0.035)”
§ Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial > Results > Exploratory and post hoc analyses
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“the p16_variant 5 assay appeared to more effectively identify individuals likely to have a favorable skeletal response to D + Q compared with the p16_variant 1 + 5 assay.”
§ Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial > Results > Exploratory and post hoc analyses
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“the secondary endpoint, percentage changes in the bone formation marker procollagen type 1 N-terminal propeptide (P1NP), increased significantly (relative to control) in the D + Q group at both 2 weeks (+16%, P = 0.020) and 4 weeks (+16%, P = 0.024), but was not different from control at 20 weeks”
§ Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial > Abstract
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“baseline SASP factors were generally higher in the T3 group versus the T1/T2 group”
§ Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial > Results > Assessment of SASP factors
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“changes in SASP factors did not differ between the control and D + Q groups”
§ Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial > Results > Assessment of SASP factors
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“in humans, senolytics (or at least, D + Q with our monthly dosing regimen) may preferentially stimulate bone formation over inhibiting bone resorption”
§ Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial > Discussion
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“radius BMD at 20 weeks, which increased by 2.7% in response to D + Q relative to control (P = 0.004) in the T3 group”
§ Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial > Results > Exploratory and post hoc analyses
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
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“Our study represents the largest (n = 60) RCT of sustained intermittent administration of a senolytic regimen to generally healthy older women.”
§ Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial > Discussion
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“our findings support the hypothesis that the skeletal, and perhaps nonskeletal, response to a senolytic intervention depends on the existing senescent cell burden.”
§ Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial > Discussion
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“intermittent D + Q treatment did not reduce bone resorption in the overall group of postmenopausal women.”
§ Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial > Abstract
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“a Phase 2 trial in postmenopausal women showed limited biomarker changes with subtle or no significant clinical improvements in bone mass37.”
From Emerging strategies in senotherapeutics: from broad-spectrum senolysis to precision reprogramming (2026) · cites this paper as [37]
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§ Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial > Discussion
“Previous studies of systemic administration of senolytics have not included a control group, recruited only a limited number of patients with diabetes-associated chronic kidney disease (n = 9)32, idiopathic pulmonary fibrosis (n = 14)33, dementia (n = 5)11 or diabetic macular edema (n = 8)12”
§ Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial > Abstract
“a single intraocular administration of another senolytic compound, the BCL-xL inhibitor UBX1325, was safe and improved visual acuity in five of eight patients with diabetic macular edema”
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In the paper
“D’Andrea, G. Quercetin: a flavonol with multifaceted therapeutic applications? Fitoterapia 106, 256–271 (2015).”
Cited work 10.1016/j.fitote.2015.09.018 · retracted 2024-12-28 · notice 10.1016/j.fitote.2024.106320 · this paper published 2024-07-02
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Mechanistic Links Between the Gut Microbiome and Longevity Therapeutics
Garzon-Escamilla, N., Medina-Cardena, M., Roy, P., Trent, J., Jamous, J., Somesan, Y., & Denslow, S. (2026) · Biomedicines · doi:10.3390/biomedicines14020316 · Cited by 5
“Moreover, ongoing clinical trials are evaluating the feasibility, safety, and tolerability of D+Q therapies for modulating AD progression, for bone loss in postmenopausal women, and to improve physical function in patients with idiopathic pulmonary fibrosis [143,144,158].”
Huang, Y., Zhou, Y., He, Z., Yang, J., Gu, J., Cui, B., Li, S., Deng, H., Zhao, W., Yang, X., et al. (2025) · Inflammation · doi:10.1007/s10753-024-02213-0 · Cited by 4
Aging and anti-aging strategies: A review of past and future therapeutics
Wei, Y., Xiong, B., Song, Z., Zhong, S., Zheng, N., Zhang, A., Chen, Y., & Sun, H. (2025) · Bioorganic & Medicinal Chemistry · doi:10.1016/j.bmc.2025.118340 · Cited by 4
Khan, T., McFall, D. J., Hussain, A. I., Frayser, L. A., Casilli, T. P., Steck, M. C., Sánchez-Brualla, I., Kuehn, N. M., Cho, M., Barnes, J. A., et al. (2025) · Annals of Neurology · doi:10.1002/ana.78118 · Cited by 5
Proteolysis targeting chimeras as senolytics: An emerging senotherapy for combating aging
Cruickshank-Taylor, A. B., Kozora, J. S., Carew, J. S., Nawrocki, S. T., & Wang, W. (2025) · The Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/j.jpet.2025.103752 · Cited by 4
Targeting Genome Stability to Mitigate Human Aging and Disease
Toiber, D., & Schumacher, B. (2025) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathmechdis-042624-105942 · Cited by 4
Growth differentiation factor 15 and the risk of hip fracture in older adults
Mattia, L., Patel, S., Webber, K., Pugliese, G., Cummings, S. R., & Eastell, R. (2026) · JBMR Plus · doi:10.1093/jbmrpl/ziaf192 · Cited by 4
Cancer and aging: complex associations and therapeutic targets
Liang, J., Zang, S., Zhe, W. A. N. G., & Zhang, R. (2026) · Molecular Biomedicine · doi:10.1186/s43556-026-00423-6 · Cited by 4
Senescent cells: a therapeutic target in correction of aging
Kirichenko, T. V., Markina, Y. V., Markin, A. M., Eremin, I. I., & Deev, R. V. (2024) · Восстановительные биотехнологии, профилактическая, цифровая и предиктивная медицина. · doi:10.17116/rbpdpm2024103153 · Cited by 4
Game changer: Navigating between challenges and hopes in geropharmacology
Chen, Q., Hartman, R., Dankiv, L., Yan, E., Young, L. H., & Barsotti, R. (2025) · Advances in pharmacology · doi:10.1016/bs.apha.2025.02.007 · Cited by 2
Devi, K., Shanmugarajan, T. S., & Ravichandiran, V. (2025) · Current Topics in Medicinal Chemistry · doi:10.2174/0115680266387622250519052501 · Cited by 2
The Role of Senolytics in Osteoporosis
Chen, E., Zhang, J., Chen, H., & Li, W. (2025) · Biomolecules · doi:10.3390/biom15081176 · Cited by 6
“…ID: NCT04313634) conducted by the Mayo Clinic demonstrated that levels of procollagen type I N-terminal propeptide (PINP) were higher in the dasatinib and quercetin treatment group at weeks 2 and 4 compared to controls, although no significant differences were observed by week 20 [135].”
Liu, Q., Xie, Z., Li, W., Li, M., & Qi, Y. (2025) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2025.1714824 · Cited by 2
The regeneration model of aging and its practical implications
Dassoff, E. (2026) · Discover Medicine · doi:10.1007/s44337-025-00558-5 · Cited by 2
CD8+ T cell aging, senescence, and related disease
He, Z., Guo, F., Zhao, Q., & Lu, W. (2026) · Science China Life Sciences · doi:10.1007/s11427-025-3101-7 · Cited by 3
Yang, Q., Xie, C., Luo, Z., Huang, W., Zhang, Z., Ren, K., Xu, X., HE, H., He, M., & Yin, L. (2026) · Redox Report · doi:10.1080/13510002.2026.2632434 · Cited by 4
“This feasibility is grounded in its established safety and tolerability profile across diverse populations, including patients with pathological conditions [25] or post-acute recovery [62], and specific subgroups of healthy individuals [63,64].”
Tagliafico, L., Canevelli, M., Barreto, P. D. S., Cesari, M., Ferrucci, L., Vellas, B. J., & Rolland, Y. (2026) · The Journal of Frailty & Aging · doi:10.1016/j.tjfa.2026.100147 · Cited by 3
“Although no overall reduction in bone resorption was observed across the entire patient cohort, a potential therapeutic response was noted among a subsample of individuals with a high burden of senescent cells [34].”
High‐Salt Diet–Induced Endothelial Dysfunction Is Mediated by Cellular Senescence
do Nascimento, A. F., Luvizotto, R. D. A. M., Costa, R. M., Pimenta, G. F., Bruder‐Nascimento, A., & Bruder-Nascimento, T. B. (2026) · Journal of the American Heart Association · doi:10.1161/jaha.125.045304 · Cited by 3
“Several clinical trials are now evaluating senolytic drugs for diverse conditions, including bone metabolism disorders, 37 Alzheimer disease, 38 and diabetic macular edema, 39 while preclinical studies have shown therapeutic benefits in models of atherosclerosis and kidney disease.”
Wen, Z. H., Yu, M., Li, S., Zeng, F., Li, J. W., Li, J. W., Liang, G., & Wang, K. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1855772 · Cited by 2
Hou, J., Chen, K.-X., Xiao, Q.-N., Hu, C., Wei, J., Jiang, Y.-Z., Liu, L., He, C., Huang, M., Jiao, Y., et al. (2026) · Nature Aging · doi:10.1038/s43587-026-01130-1 · Cited by 4
“Moreover, recent clinical studies have further confirmed that D+Q therapy demonstrated feasibility, safety and tolerability in mild Alzheimer’s disease 18 and postmenopausal osteoporosis 19 .”
Systemic recalibration and epigenetic resetting as complementary strategies in ageing biology
Li, Y.-Y., & Tay, F. R. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103227 · Cited by 2
Laohajaroensombat, O., Poochanasri, M., & Samakkarnthai, P. (2025) · Current Opinion in Endocrinology Diabetes and Obesity · doi:10.1097/med.0000000000000915 · Cited by 1
Gao, X., Ruzbarsky, J. J., Huard, M., Sajedi, S., Shyu, P. T., Xiao, Z., Force, B. S., White, S., Ayers, J. D., Wang, B., et al. (2025) · Pharmacological Research · doi:10.1016/j.phrs.2025.108016 · Cited by 1
“A recent clinical trial also demonstrated that D+Q did not significantly reduce bone resorption in post-menopausal women despite its effectiveness in decreasing osteoclasts in aged mice [34,54].”
Deconstructing senescence phenotypes in cells of the bone and bone marrow
Hofbauer, L. C., & Rauner, M. (2026) · Journal of Clinical Investigation · doi:10.1172/jci204645 · Cited by 2
“While the overall study did not meet the endpoints, senolysis with dasatinib/quercetin significantly improved bone markers and increased bone mineral density at the radius in those women with the highest senescent cell burden, determined by p16 + T cells (9).”
Ceramic-based biomaterials: Combining regeneration with anti-senescence
Ma, X., Yang, Z., Jin, K., Cao, S., Ma, B., Xiao, Y., & Wu, C. (2026) · Biomaterials · doi:10.1016/j.biomaterials.2026.124195 · Cited by 1
From systemic disease to the eye: Why senescence deserves attention in ocular infections
Maiti, S., & Joseph, J. (2026) · Experimental Eye Research · doi:10.1016/j.exer.2026.111095 · Cited by 1
The gut-bone-inflammation axis: intestinal barrier disruption as a central driver of osteoporosis
Liu, X., Hu, K., & Zhu, T. (2026) · Osteoporosis International · doi:10.1007/s00198-026-07855-4 · Cited by 3
Civitelli, R. (2026) · Journal of Bone and Mineral Research · doi:10.1093/jbmr/zjag042 · Cited by 1
Senotherapeutics: Emerging pharmacological strategies to target cellular senescence
Nagy, D., Brunner, E., Ekambaram, S., Nagaraja, R. Y., Kordestan, K. V., Patai, R., Kristóf, R., Nagykaldi, M., Chandragiri, S. S., Shanmugarama, S., et al. (2026) · Advances in Translational Research · doi:10.1556/1661.2026.00015 · Cited by 1
Clinical Features of Cellular Senescence Pathways in Severe Asthma
Song, W., Kermani, N. Z., Versi, A., Sánchez‐Ovando, S., Simpson, J. L., Wark, P. A., Baines, K. J., Dahlén, S., Djukanović, R., Guo, Y., et al. (2026) · Allergy · doi:10.1111/all.70416 · Cited by 1
The immunology behind inflammaging—causes, sources, and mechanisms
Sturmlechner, I., LeBrasseur, N. K., Weyand, C. M., & Goronzy, J. J. (2026) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2026.05.031 · Cited by 3
Self-citationCellular Senescence and Aging: Mechanisms, Disease Convergence, and Therapeutic Frontiers
Cai, G., Ren, J., Wang, L., Wu, Y., Wang, H., Cao, X., Shang, H., Hou, X., Wang, Y., Xue, H., et al. (2026) · MedComm · doi:10.1002/mco2.70827 · Cited by 2
Aging of mesenchymal stem cells in bone aging: Mechanisms, impact, and therapeutic perspectives
Zhou, Z., Wang, H. W., Jin, Z., Wen, B., Wu, T., Zhu, T., & Liu, D. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103240 · Cited by 4
Osteoimmune senescence in aging-related bone diseases
Li, H., Yang, Y., & Zhu, H. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1892334 · Cited by 5
Geng, Q., Geng, Y., Heng, K., Zhai, J., Song, X., Sha, L., Geng, Y., Nie, P., Liu, F., Zhai, H., et al. (2025) · Journal of Translational Medicine · doi:10.1186/s12967-025-07212-9 · Cited by 1
“Cellular senescence is a hallmark of aging and a significant driver of various chronic diseases, including diabetes, cardiovascular disease, kidney disease, Alzheimer’s disease, and osteoporosis [13, 20, 27, 29, 36].”
Urrego, C. A., Sexton, B., & Kohn, D. H. (2025) · Bone · doi:10.1016/j.bone.2025.117665
Tan, J., Zhu, J., He, Y., Fan, Z., Cai, F., Zhuang, H., Hu, Y., Liu, K., Li, Q., Feng, B., et al. (2025) · BMC Musculoskeletal Disorders · doi:10.1186/s12891-025-09298-0
“…interventions targeting mitochondrial homeostasis in bone cells [40] and senolytic therapies aimed at reducing the load of senescent cells in post-menopausal women [41], could complement early detection efforts by targeting the underlying biological processes that drive bone aging and osteoporosis.”
Partial Reprogramming Is Conserved from Insect to Mammal
Tolwinski, N. S., Fong, S., Shankar, S., & Gruber, J. (2026) · Cells · doi:10.3390/cells15020168
“However, early increases in bone-formation markers were observed, especially among participants with higher baseline senescent-cell burden, indicating a potentially biology-dependent response to senolytic therapy [100].”
Transplanting ANXA1⁻ CD8⁺ Naïve T cells Delay Aging Through SenolysisPreprint
Wu, Y., Guo, S. Z., Zhang, F., Lou, F., Li, Y. Y., Sun, Y., Shen, Q., Zhao, L., Cai, X., Wang, Z., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.02.21.707223
Chronic low-grade inflammation and primary osteoporosis
Štěpán, J. (2025) · Clinical Osteology · doi:10.36290/clo.2025.023
Multifacet Roles of Cellular Senescence in Cancer: Mechanisms and Therapeutic Implications
Mao, H., Liu, W., Su, Y., Ma, Y., Zhao, X., & Lu, Y. (2026) · MedComm – Oncology · doi:10.1002/mog2.70060 · Cited by 1
SENOLYTIC COMBINATION OF DASATINIB AND QUERCETIN: A REVIEW OF PRECLINICAL AND CLINICAL STUDIES
Morozov, I. I., Molkanov, N. N., & Kiseleva, N. M. (2025) · Медико-фармацевтический журнал «Пульс» · doi:10.26787/nydha-2686-6838-2026-28-1-49-58
Blomquist, S. A., Kelly, G., D’Adamo, C. R., Han, C., Parker, H., Adães, S., Gardner, C. R., Ardagh, A., Ramer, S., & Scuba, W. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27104406 · Cited by 1
“On the other hand, two human studies evaluating dasatinib and quercetin in idiopathic pulmonary fibrosis and in post-menopausal individuals have failed to show significant alteration of SASP markers at the population level [58,59].”
Liu, Y., O’Brien, E. M., Lottinger, C., Perumal, G., Spiller, K. L., & Kuhn, L. T. (2026) · Research Square · doi:10.21203/rs.3.rs-9624236/v1
“Clinical trials of patients taking senolytics and/or senomorphics systemically (orally or by injection) on a continuous basis for osteoporosis management show a moderate benefit 21 .”
Integrating senotherapeutics into transplantation: liver reconditioning in an aging donor pool
Buch, M. L., Esser, H., Perera, H., Zheng, R., Ferreira-González, S., & Forbes, S. J. (2026) · Transplant International · doi:10.3389/ti.2026.16347
“A landmark Phase II randomized controlled trial demonstrated that response to D + Q is influenced by baseline SnC burden, with significant benefits in individuals with high p16 INK4 expression [116].”
Liu, Z., Abulaiti, A., Li, D., Li, J., Wahafu, P., Zhang, Y., Maimaitiming, M., Li, S. Y., Li, G., & Yakufu, M. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103221
Ageing-driven periodontitis: molecular mechanisms and emerging anti-ageing interventions
Li, M. M., Peng, Z., Wang, R., Zheng, Y., Li, S., Kreher, D., Schmalz, G., Han, Q., & Tang, H. (2026) · European journal of medical research · doi:10.1186/s40001-026-04846-3
“However, in terms of clinical data, a recent phase II clinical trial in postmenopausal women (for systemic bone loss) revealed that the improvement in human bone metabolism by D + Q was more limited and transient than that in mouse models [126].”
Mechanism and regulation of programmed cell death in aging-related diseases
Xie, X., & Xu, D. (2026) · Cell chemical biology · doi:10.1016/j.chembiol.2026.06.005 · Cited by 1
From local to systemic: Spinal aging in the multi-organ aging network
Zhang, C., 彭舒畅, Fu, J., Du, Y., Qian, Y., Song, Y., Wang, K. J., & Yang, C. G. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103253
Fehlgeleitete interzelluläre Kommunikation beim Altern und bei chronischen Entzündungen
Großkopf, A., Saemann, L., & Simm, A. (2026) · Zeitschrift für Gerontologie und Geriatrie · doi:10.1007/s00391-026-02619-5
Song, Y., Zhang, R., Zhang, X., Wang, J., Chen, J., & Li, L. (2026) · Frontiers in Chemistry · doi:10.3389/fchem.2026.1861883
“Nevertheless, its feasibility will depend on demonstrating skeletal targeting, optimal dosing intervals, safety, and appropriate treatment sequencing, particularly in light of the limited overall benefit observed in the Phase II D + Q trial (Farr et al., 2024).”
InfluentialCorticotropin-releasing factor (CRF) in brain aging: from mitochondrial dysfunction to inflammaging
Yan, M., Hua, L., Jiang, J., Wu, J., Zeng, Z., He, Y., & Chen, Y. (2026) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2026.1880569
Toward a context-aware geroscience: integrating structural and social context into aging biology
Bellizzi, K. M., Kuchel, G. A., Redeker, N. S., & Nwakasi, C. C. (2026) · The Gerontologist · doi:10.1093/geront/gnag179
Metadata
- Authors
- 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., Doolittle, M. L., Bancos, I., Yu, K., Tchkonia, T., LeBrasseur, N. K., Kirkland, J. L., Monroe, D. G., & Khosla, S.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Farr, Joshua N.
- Khosla, Sundeep
- ORCID
- Venue
- Nature Medicine
- Published
- 2024-07-02
- Volume
- 30
- Issue
- 9
- Pages
- 2605-2612
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC11705617
- OpenAlex
- W4400248879
- Semantic Scholar
- 0e53cd07806a2b8dfab4ce0f5781c7d52dcac991
- Cited by
- 127
- References
- 39
- Citations by year
- 2026: 67 · 2025: 55 · 2024: 5
- FWCI
- 35.85
- Type
- journal article
- Language
- en
- Open access
- green
- pmc.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Medicine (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- Digital Commons-TMC (Texas Medical Center) (submittedVersion)
- Funders
- U.S. Department of Health & Human Services | NIH | National Institute on Aging (R21 AG065868, R01 AG076515, R01 AG055529, R37 AG13925, R33 AG61456, P01 AG062413, R01 AG 062413)
- U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK128552)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Keywords
- senolytics, intermittent dosing, dasatinib, quercetin, bone metabolism, postmenopausal women, bone loss, bone resorption, bone formation, C-terminal telopeptide of type I collagen, P1NP, CDKN2A, bone mineral density, aging
- MeSH terms
- Dasatinib, Senotherapeutics, Aged, Bone and Bones, Bone Resorption, Female, Humans, Middle Aged, Peptide Fragments, Peptides, Procollagen, Quercetin, Biomarkers, Bone Density, Cellular Senescence, Postmenopause, Cyclin-Dependent Kinase Inhibitor p16, Collagen Type I
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