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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Claims the paper makes
- Finding
In exploratory analyses, the highest tertile of T cell p16 mRNA levels showed increases in P1NP and reductions in CTx after D + Q treatment.
“serum P1NP increased at 2 weeks in the T3 D + Q group (relative to control, +34%, P = 0.035)”
Quote in the paperNot yet classified - Finding
The authors conclude that the p16_variant 5 assay more effectively identified individuals likely to have a favorable skeletal response to D + Q than the p16_variant 1 + 5 assay.
“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.”
Quote in the paperNot yet classified - Finding
The trial found that D + Q increased the bone formation marker P1NP at 2 and 4 weeks, but not at 20 weeks, in the overall group.
“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”
Quote in the paperNot yet classified - Finding
Baseline SASP factors were generally higher in the T3 group than in the T1/T2 group.
“baseline SASP factors were generally higher in the T3 group versus the T1/T2 group”
Quote in the paperNot yet classified - Finding
In the T3 group, changes in SASP factors did not differ between the control and D + Q groups.
“changes in SASP factors did not differ between the control and D + Q groups”
Quote in the paperNot yet classified
- Finding
The authors note that intermittent D + Q may preferentially stimulate bone formation over inhibiting bone resorption in humans.
“in humans, senolytics (or at least, D + Q with our monthly dosing regimen) may preferentially stimulate bone formation over inhibiting bone resorption”
Quote in the paperNot yet classified - Finding
In exploratory analyses, the highest tertile of T cell p16 mRNA levels showed an increase in radius BMD at 20 weeks after D + Q treatment.
“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”
Quote in the paperNot yet classified - Finding
The authors state that the study was the largest RCT of sustained intermittent senolytic administration in generally healthy older women.
“Our study represents the largest (n = 60) RCT of sustained intermittent administration of a senolytic regimen to generally healthy older women.”
Quote in the paperNot yet classified - Finding
The trial's exploratory analyses suggest that the skeletal response to senolytic therapy depends on the underlying senescent cell burden.
“our findings support the hypothesis that the skeletal, and perhaps nonskeletal, response to a senolytic intervention depends on the existing senescent cell burden.”
Quote in the paperNot yet classified - Finding
The trial found that intermittent D + Q did not reduce bone resorption in the overall group of postmenopausal women.
“intermittent D + Q treatment did not reduce bone resorption in the overall group of postmenopausal women.”
Quote in the paperNot yet classified - Finding
No serious adverse events were observed in the trial.
“No serious adverse events were observed.”
Quote in the paperNot yet classified - Method
The study compared D + Q with control over 20 weeks in 60 postmenopausal women.
“We conducted a 20-week, phase 2 RCT comparing D + Q with control for improving bone turnover markers in 60 postmenopausal women.”
Quote in the paperNot yet classified - Method
The investigators measured 36 SASP factors at baseline and 2 weeks postdosing in additional analyses.
“we measured a panel of 36 SASP factors at baseline and 2 weeks postdosing.”
Quote in the paperNot yet classified - Method
The investigators hypothesized that women with a higher baseline senescent cell burden would be more likely to respond to a senolytic intervention.
“We hypothesized that women with a high basal senescent cell burden would be more likely to respond to a senolytic intervention”
Quote in the paperNot yet classified - Method
The primary endpoint was the percentage change in serum CTx from baseline over 20 weeks.
“The primary study endpoint was the percentage change in CTx from baseline over 20 weeks.”
Quote in the paperNot yet classified - Method
Secondary endpoints included changes in serum P1NP, serum CTx at 2, 4 and 20 weeks, BMD by DXA, and safety, tolerability and circulating SASP factors.
“Secondary endpoints included changes in serum P1NP, as well as in serum CTx at 2, 4 and 20 weeks. In addition, we assessed percentage changes in BMD by DXA (radius, femur neck and lumbar spine) at 20 weeks. Additional endpoints were safety, tolerability and circulating SASP factors.”
Quote in the paperNot yet classified - Method
Eligible participants were women older than 60 years with T cell p16 mRNA levels above the 95th percentile of young control women.
“we selected women aged >60 years with a senescent cell burden based on p16 mRNA expression in peripheral blood T cells greater than the 95th percentile of young control women aged 22–31 years.”
Quote in the paperNot yet classified - Method
The study used an open-label design because over-encapsulating the medications to ensure double-blinding was cost-prohibitive.
“over-encapsulating all study medications to ensure double-blinding proved to be cost-prohibitive so, in this initial ‘proof-of-concept’ study, we elected to use an open-label design”
Quote in the paperNot yet classified - Method
The study was a phase 2 randomized controlled trial of intermittent dasatinib plus quercetin in postmenopausal women.
“we conducted a phase 2 randomized controlled trial of intermittent administration of the senolytic combination dasatinib plus quercetin (D + Q) in postmenopausal women”
Quote in the paperNot yet classified - Method
T cell p16 mRNA was measured at baseline in CD3+ peripheral blood T cells by qPCR.
“At baseline, morning fasting peripheral whole blood (10 ml) was obtained from the participants for measuring p16 mRNA in CD3+ peripheral blood T cells via qPCR.”
Quote in the paperNot yet classified - Method
D + Q was administered orally on an intermittent schedule every 28 days over 20 weeks for five dosing sessions.
“D + Q was taken orally on an intermittent schedule with no-therapy periods in between doses, repeated every 28 days over 20 weeks, resulting in five total dosing sessions throughout the entire intervention”
Quote in the paperNot yet classified - Method
The trial monitored withdrawals and adverse events and used the Common Terminology Criteria for Adverse Events for reporting.
“We monitored and rigorously documented all participants who withdrew from the study, the reasons for withdrawal and all adverse events (serious and nonserious).”
Quote in the paperNot yet classified - Background
The abstract describes preclinical evidence that senescent cells accumulate with aging and that senolytics delay multiple age-related morbidities, including bone loss.
“Preclinical evidence demonstrates that senescent cells accumulate with aging and that senolytics delay multiple age-related morbidities, including bone loss.”
Quote in the paperNot yet classified - Method
The study randomized 60 eligible postmenopausal women aged 60 to 90 years to control or D + Q.
“We randomized 60 eligible postmenopausal women (follicle-stimulating hormone >20 IU l−1; sex/gender based on self-reporting) aged 60–90 years to one of two groups: control or D + Q.”
Quote in the paperNot yet classified
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Intraocular study counted as systemic administration
MinorThe discussion includes the diabetic macular edema study among prior studies of systemic senolytic administration, but the paper earlier describes that treatment as a single intraocular injection.
“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”
“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”
Cited works that were retracted
Works this paper cites that were later retracted, from the retraction notices publishers deposit. Major when the notice came out before this paper was published.
Cites a retracted work: 10.1016/j.fitote.2015.09.018
InfoThe cited work was retracted on 2024-12-28 (notice 10.1016/j.fitote.2024.106320), not before this paper was published (2024-07-02).
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
“D’Andrea, G. Quercetin: a flavonol with multifaceted therapeutic applications? Fitoterapia 106, 256–271 (2015).”
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RETRACTED: Quercetin: A flavonol with multifaceted therapeutic applications?
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Advances in the management of osteoporosis
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InfluentialSelf-citationImmune Aging in Rheumatoid Arthritis
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“18 Another class of SASP-targeting drugs are the senomorphics, designed to modify SASP factors in vivo.”
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Recent Advances in Osteoporosis Therapeutics
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A Critical Appraisal of the Utility of Targeting Therapy-Induced Senescence for Cancer Treatment
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Characterization of Human Senescent Cell Biomarkers for Clinical Trials
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Dasatinib and Quercetin Mitigate Age‐Related Alveolar Bone Inflammaging and Neutrophil Infiltration
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Self-citationSenescence of skeletal stem cells and their contribution to age-related bone loss
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“Comparison studies were performed with the clinically common combination treatment using D + Q ( 6 , 35 , 36 ).”
Biomarkers of Cellular Senescence in Type 2 Diabetes Mellitus
Hoong, C. W. S., Farr, J. N., Monroe, D. G., White, T. A., Atkinson, E. J., Tweed, A. J., Palmer, A. K., LeBrasseur, N. K., Sfeir, J. G., & Khosla, S. (2025) · Aging Cell · doi:10.1111/acel.70120 · Cited by 10 · see citing works
Self-citationTranslating cellular senescence research into clinical practice for metabolic disease
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“…pilot trials have shown that senescent cells can be cleared in humans both in tissues and systemically 28 , senolytics are well tolerated (as shown in multiple trials) and, most importantly, individuals with high senescent cell burden seem to benefit the most from senolytic therapies 81,167,168 .”
Self-citationColonic Aging and Colorectal Cancer: An Unignorable Interplay and Its Translational Implications
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“Biomarkers like plasma IL-6, TNF-alpha, and GDF15 (components of SASP) are measured to monitor the effectiveness of these treatments and the systemic senescent burden in trials for conditions like idiopathic pulmonary fibrosis, osteoarthritis, and Alzheimer’s disease [182].”
Falvino, A., Bonanni, R., Tarantino, U., Tancredi, V., & Cariati, I. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26157573 · Cited by 11 · see citing works
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InfluentialCai, Z., Wang, H., Hu, J., Qu, C., Chen, S., Liu, X., & Fan, C. (2025) · The American Journal of Sports Medicine · doi:10.1177/03635465251381763 · Cited by 10 · see citing works
Functional Features of Senescent Cells and Implications for Therapy
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Kontoghiorghes, G. J. (2025) · Nutrients · doi:10.3390/nu17203270 · Cited by 9 · see citing works
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Cellular senescence in age-related musculoskeletal diseases
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“Moreover, recent clinical trials have demonstrated the efficacy of senolytic therapy in promoting osteogenesis. however, its capacity to inhibit osteoclast activity is limited [36].”
Towards a personalized approach in senolytic trials
Khosla, S., Monroe, D. G., & Farr, J. N. (2025) · Nature Aging · doi:10.1038/s43587-025-00964-5 · Cited by 6 · see citing works
Self-citationEffect of senolytic drugs in young female mice chemically induced to estropause
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Targeting senescent microglia in progressive multiple sclerosis: a geroscience-informed approach
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Senotherapeutics for metabolic disease and diabetic complications
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“Clinical trials of senolytics for Alzheimer’s disease and age-related osteoporosis suggest early promise [141–144].”
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“No consistent alterations in systemic iron indices have been reported in the D+Q trials, although both quercetin and dasatinib possess metal-binding ligands [14], and quercetin itself possesses iron-binding and antioxidant properties that may contribute to its senomorphic actions [14,263,264].”
Insights into the therapeutic strategies for aging and aging-associated diseases
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“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].”
Emerging strategies in senotherapeutics: from broad-spectrum senolysis to precision reprogramming
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Targeting Genome Stability to Mitigate Human Aging and Disease
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Growth differentiation factor 15 and the risk of hip fracture in older adults
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Cancer and aging: complex associations and therapeutic targets
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Senescent cells: a therapeutic target in correction of aging
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The Role of Senolytics in Osteoporosis
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“…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].”
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CD8+ T cell aging, senescence, and related disease
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“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].”
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“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
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“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.”
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“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
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“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
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“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 · see citing works
From systemic disease to the eye: Why senescence deserves attention in ocular infections
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The gut-bone-inflammation axis: intestinal barrier disruption as a central driver of osteoporosis
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Clinical Features of Cellular Senescence Pathways in Severe Asthma
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The immunology behind inflammaging—causes, sources, and mechanisms
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Self-citationCellular Senescence and Aging: Mechanisms, Disease Convergence, and Therapeutic Frontiers
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Aging of mesenchymal stem cells in bone aging: Mechanisms, impact, and therapeutic perspectives
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Osteoimmune senescence in aging-related bone diseases
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“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
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 · see citing works
“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 · see citing works
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
- 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
- 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
- Health Sciences › Medicine › Physiology › 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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