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JAK inhibition alleviates the cellular senescence-associated secretory phenotype and frailty in old age
Open accessAbstract
Significance: A hallmark of aging is chronic sterile inflammation, which is closely associated with frailty and age-related diseases. We found that senescent fat progenitor cells accumulate in adipose tissue with aging and acquire a senescence-associated secretory phenotype (SASP), with increased production of proinflammatory cytokines compared with nonsenescent cells. These cells provoked inflammation in adipose tissue and induced macrophage migration. The JAK pathway is activated in adipose tissue with aging, and the SASP can be suppressed by inhibiting the JAK pathway in senescent cells. JAK1/2 inhibitors reduced inflammation and alleviated frailty in aged mice. One possible mechanism contributing to reduced frailty is SASP inhibition. Our study points to the JAK pathway as a potential target for countering age-related dysfunction.
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“Sncs can directly cause insulin resistance through release of SASP factors such as IL-6 and TNF-α (39, 40).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [39]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“We showed that aged 3xTg-AD male mice in particular, exhibit elevated plasma levels of known SASP factors [65, 66], including IL-12, IL-10, IL-6, CXCL2, CXCL1, and G-CSF”
From Age, sex and Alzheimer’s disease: a longitudinal study of 3xTg-AD mice reveals sex-specific disease trajectories and inflammatory responses mirrored in postmortem brains from Alzheimer’s patients (2024) · cites this paper as [66]
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“This concept is supported by a study of aged mice demonstrating that pharmacologic inhibition of the JAK pathway, which regulates the SASP in senescent preadipocytes and endothelial cells in vitro, suppresses markers of both adipose tissue and systemic inflammation and improved parameters of muscle strength, endurance, and coordination (39).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [39]
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“Furthermore, JAK inhibitors alleviated frailty in aged mice99.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [99]
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“Similarly, other inhibitors of proinflammatory signalling (e.g. JAK/STAT [124] and p38 [60]) and antibodies targeting IL-6 [125], IL-1 [126] and TNFa [127], might be potentially effective senomorphic drugs.”
From The role of cellular senescence and SASP in tumour microenvironment (2023) · cites this paper as [124]
In the citing paper
“Alternatively, it is possible to modulate individual components of the SASP by inhibiting Janus kinase (JAK) 1/2148 and JAK2/signal transducer and activator of transcription 3 (STAT3).149”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [148]
In the citing paper
“Similarly, the inhibition of pro-inflammatory JAK signalling in the same model was shown to attenuate pathogenesis by reducing the infiltration of monocytes to the lung130–132.”
From COVID-19 and cellular senescence (2023) · cites this paper as [131]
In the citing paper
“However, senomorphic treatment may require continuous administration and could potentially disrupt tissue homeostasis due to SASP blockade.”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [192]
In the citing paper
“In terms of alleviating age-related phenotypes, minimizing the SASP using Janus kinase/signal transducer and activator of transcription (JAK/STAT) inhibition is very similar to eliminating or reducing the burden of senescent cells genetically (e.g., using INK-ATTAC mice) or pharmacologically with senolytic agents [4, 11, 13, 60].”
From Reducing Senescent Cell Burden in Aging and Disease (2020) · cites this paper as [13]
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Russo, L., Babboni, S., Andreassi, M. G., Daher, J., Canale, P., Turco, S. D., & Basta, G. (2025) · Antioxidants · doi:10.3390/antiox14010099 · Cited by 16
“The inhibition of activin A in senescent cells has been shown to restore adipogenic capabilities in progenitor cells, suggesting a potential therapeutic target to counteract age-related metabolic decline [80,81].”
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“In addition, as the Janus kinase (JAK)/ STAT pathway is a critical regulator of the SASP, ruxolitinib, which is a pharmacological inhibitor of JAK and is used for the treatment of intermediate or high-risk myelofibrosis, has been reported to suppress senoinflammation in vitro and alleviate age-related tissue dysfuncti…”
BackgroundBian, X., Snow, Z. K., Zinn, C. J., Gowan, C. C., Conley, S. M., Bratulin, A. L., Elhusseiny, K. M., Miller, J. D., Tchkonia, T., Kirkland, J. L., et al. (2025) · Kidney360 · doi:10.34067/kid.0000000776 · Cited by 13
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Self-citationWang, C., Liu, X., Zhou, J., & Zhang, Q. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25021126 · Cited by 15
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Future Directions of Therapeutic Vaccines for Chronic Diseases
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Senescent Cells: Dual Implications on the Retinal Vascular System
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“To investigate the role of the JAK-STAT pathway in age-related inflammation, Xu et al. performed a series of experiments and demonstrated that inhibition of the JAK-STAT signaling pathway suppresses the SASP in aged preadipocytes and human umbilical vein endothelial cells (HUVECs) [92].”
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Young gut microbiota transplantation improves the metabolic health of old mice
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“[125,127]”
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InfluentialAssociation of frailty with clinical outcomes in myelofibrosis: a retrospective cohort study
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Tripathi, U., Suda, M., Kulshreshtha, V., Piatkowski, B. T., Palmer, A. K., Giorgadze, N., Inman, C. L., Gasek, N. S., Xu, M., Johnson, K. O., et al. (2025) · Aging Cell · doi:10.1111/acel.70358 · Cited by 10
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Saemann, L., Naujoks, P., Hartrumpf, L., Pohl, S., Simm, A., & Szabo, G. B. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241411727 · Cited by 10
“Due to the ability to block the release of several cytokines, ruxolitinib has also been used as a senotherapeutic drug [9].”
Roles of Protein Post-Translational Modifications During Adipocyte Senescence
Hwang, M.-S., Park, J., Ham, Y., Lee, I. H., & Chun, K. (2023) · International Journal of Biological Sciences · doi:10.7150/ijbs.86404 · Cited by 11
“Action site Phosphorylation JAK [34, 36, 37] SASP JAK/STAT pathway P38 MAPK [40-42] IRS-2 p38 MAPK signaling pathway Dephosphorylation PTEN [49-51] PIP3 PI3K/AKT signaling pathway D3 Deacetylation SIRT1 [57,58,62] PPARγ Lipogenesis Lys 268 and Lys293 SIRT6 [64] p27 Kip1 Adipocyte differentiation…”
BackgroundExercise Alleviates Aging of Adipose Tissue through Adipokine Regulation
Jia, D., Zhang, H., Liu, T., & Wang, R. (2024) · Metabolites · doi:10.3390/metabo14030135 · Cited by 12
“Adipose-derived stem cells from older donors exhibited heightened expression of p16 Ink4a , which significantly contributes to reduced cellular differentiation [28].”
BackgroundSingle-cell multi-omics identify novel regulators required for osteoclastogenesis during aging
Li, H., Xu, W., Tan, J.-C., Hong, Y.-M., He, J., Zhao, B.-P., Zhou, J., Zheng, Y.-M., Lei, M., Zheng, X., et al. (2024) · iScience · doi:10.1016/j.isci.2024.110734 · Cited by 12
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“Xu et al. reported inhibiting the JAK/STAT pathway mitigates SASP in preadipocytes and ECs [46].”
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“Another complexity is that some drugs/compounds affect expression of senescent-associated secretory phenotype (SASP) factors without eliminating the senescent cells (Tilstra et al., 2012; Laberge et al., 2015; Xu et al., 2015).”
BackgroundOlascoaga, S., Gutiérrez, H., Königsberg, M., Pérez‐Villanueva, J., & López‐Díazguerrero, N. E. (2022) · Biogerontology · doi:10.1007/s10522-022-09974-x · Cited by 11
“While senotherapeutics is a new field with successful results in clinical trials (Xu et al. 2015; Justice et al. 2019), the structural and functional properties that determine their specific activities as either senolyt-ics or senomorphics remain unclear.”
BackgroundJAK/STAT signaling pathway gene expression is reduced following Nelf knockdown in GnRH neurons
Ko, E. K., Chorich, L. P., Sullivan, M. E., Cameron, R. S., & Layman, L. C. (2017) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2017.10.009 · Cited by 10
Cellular senescence in neurodegenerative diseases
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Associations of Frailty with Neuropsychiatric Symptoms of Alzheimer’s Disease: A Longitudinal Study
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“Existing studies have found that frailty often accompanies the accumulation of senescent cells, the loss of tissue regenerative potential [50, 51], inflam-matory activity, and oxidative stress [52–54], all of which may trigger neuronal loss and ultimately lead to the occurrence of NPSs.”
Prevention of Chronic Kidney Disease and Its Complications in Older Adults
Tungsanga, S., & Bello, A. K. (2024) · Drugs & Aging · doi:10.1007/s40266-024-01128-7 · Cited by 9
“Senostatic drugs such as metformin [45], ruxolitinib (a JAK inhibitor) [46], and rapamycin (an mTOR inhibitor) [47], among others, have shown the ability to suppress SASP and inhibit cell senescence in in vitro studies.”
Desiderio, A., Pastorino, M., Campitelli, M., Prevenzano, I., Palma, F. D. E. D., Spinelli, R., Parrillo, L., Longo, M., Milone, M., Miele, C., et al. (2024) · The FASEB Journal · doi:10.1096/fj.202401470r · Cited by 10
“…cell senescence triggered by different hits hamper APC differentiation into fully functional adipocytes and leads to the acquisition of the senescence-associated secretory phenotype (SASP), 8 which exacerbates local inflammation and impairs the function of neighboring cells in the adipose tissue.”
Body Composition and Senescence: Impact of Polyphenols on Aging-Associated Events
dos Santos, T. W., Pereira, Q. C., Fortunato, I. M., Oliveira, F. D. S., Alvarez, M. C., & Ribeiro, M. L. (2024) · Nutrients · doi:10.3390/nu16213621 · Cited by 10
“These reports corroborate the findings in adipose tissue, in which mesenchymal progenitor cells showed a loss of adipogenic potential with advancing age, while the clearance of senescent adipogenic progenitor cells restored metabolic health and adipogenesis [102,137].”
BackgroundResultPignolo, R. J., & Chandra, A. (2025) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2025.112025 · Cited by 10
Wang, Z., Chen, C., Ai, J., Gao, Y., Wang, L., Xia, S., Jia, Y., & Qin, Y. (2025) · MedComm · doi:10.1002/mco2.70048 · Cited by 12
Current strategies for senescence treatment: Focused on theranostic performance of nanomaterials
Cong, Y., Li, X., & Hong, H. (2025) · Journal of Controlled Release · doi:10.1016/j.jconrel.2025.113710 · Cited by 9
Cellular senescence in age-related musculoskeletal diseases
Xiong, J., Guo, Q., & Luo, X. (2025) · Frontiers of Medicine · doi:10.1007/s11684-025-1125-7 · Cited by 10
Aging immunity: unraveling the complex nexus of diet, gut microbiome, and immune function
Babakhani, K., Kucinskas, A. L., Ye, X., Giles, E. D., & Sun, Y. (2025) · Immunometabolism · doi:10.1097/in9.0000000000000061 · Cited by 12
Unveiling the link: aging and its impact on ocular diseases
Wang, K., Xie, Y., Lin, Y., Zhu, R., Gao, T., Han, Z., Yang, Z., Jiang, X., Chen, H., Wu, Z., et al. (2025) · Experimental Eye Research · doi:10.1016/j.exer.2025.110551 · Cited by 12
Liu, W., Fan, B., Fang, T., Li, H., Zhang, J., Liu, B., & Liu, Z. (2025) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2025.08.010 · Cited by 10
“The JAK/ STAT pathway is highly upregulated in senescent cells and tumor cells compared to normal cells 213,214 .”
Endothelial Dysfunction and Therapeutic Advances in Chronic Kidney Disease
Liang, F., Gui, L., Chen, K., Chen, J., He, J., & He, Y. (2025) · Diabetes/Metabolism Research and Reviews · doi:10.1002/dmrr.70086 · Cited by 11
“Senomorphic compounds (e.g., rapamycin, ruxolitinib and metformin) have entered clinical trials for other indications [120, 121], but their application in CKD specifically remains investigational.”
Aging and lung diseases: Unraveling mechanisms and therapeutic targets
Zhou, Y., Chen, G., Li, X., Li, X., Lin, Z., Liu, L., Pu, D., Chen, J., Chen, Y., Lin, Z., et al. (2025) · Chinese Medical Journal - Pulmonary and Critical Care Medicine · doi:10.1016/j.pccm.2025.11.005 · Cited by 10
“…(JAK–STAT) and mitogen-activated protein kinase (MAPK) (extracellular signal-regulated kinase [ERK]/JNK/p38) cascades that collectively orchestrate the transcription of proinflammatory mediators and perpet-uate inflammatory signaling, 224–226 and sustain a persistent low-grade inflammatory state.”
Zhang, Y., Yu, X., Zhou, C., Fu, K., Luo, H., & Wu, C. (2023) · Frontiers in Medicine · doi:10.3389/fmed.2023.1288993 · Cited by 9
Jiang, A., Liu, Y., Zhu, B., Fang, Y., Qu, L., Yang, Q., Luo, P., Cai, C., & Wang, L. (2024) · Clinical Genitourinary Cancer · doi:10.1016/j.clgc.2024.01.005 · Cited by 9
Senotherapeutics and HIV-1 Persistence
Szaniawski, M. A., & Spivak, A. M. (2020) · Current HIV/AIDS Reports · doi:10.1007/s11904-020-00496-0 · Cited by 9
Potential Therapies to Protect the Aging Heart Against Ischemia/Reperfusion Injury
Díaz‐Vesga, M. C., Zúñiga-Cuevas, Ú., Ramírez-Reyes, A., Herrera-Zelada, N., Palomo, I., Bravo, R., & Riquelme, J. A. (2021) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2021.770421 · Cited by 9
“It has been reported that inhibition of JAK in old mice has been linked with reduced senescence-associated secretory phenotype and frailty (65).”
BackgroundThe shades of grey in adipose tissue reprogramming
Qi, Y., & Hui, X. H. (2022) · Bioscience Reports · doi:10.1042/bsr20212358 · Cited by 9
The Possible Role of Β-Cell Senescence in the Development of Type 2 Diabetes Mellitus
Novoselova, E. G., Lunin, S. M., Khrenov, M. O., Glushkova, O. V., Novoselova, T. V., & Parfenyuk, S. B. (2023) · Cellular Physiology and Biochemistry · doi:10.33594/000000606 · Cited by 11
Doshida, Y., Hashimoto, S., Iwabuchi, S., Takino, Y., Ishiwata, T., Aigaki, T., & Ishigami, A. (2023) · Scientific Reports · doi:10.1038/s41598-023-41352-6 · Cited by 9
Aging, Cellular Senescence, and Kidney Fibrosis
Susnik, N., Sen, P., Melk, A., & Schmitt, R. (2017) · Current Pathobiology Reports · doi:10.1007/s40139-017-0143-9 · Cited by 9
Ham, M., Cho, Y., Kang, T., Oh, T., Kim, H., & Kim, K. (2024) · Aging Cell · doi:10.1111/acel.14049 · Cited by 8
Network of extracellular vesicles surrounding senescent cells
Okawa, H., Tanaka, Y., & Takahashi, A. (2024) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2024.109953 · Cited by 8
Senescence- and Immunity-Related Changes in the Central Nervous System: A Comprehensive Review
Feng, H., Li, J., Wang, H., Wei, Z., & Feng, S. (2024) · Aging and Disease · doi:10.14336/ad.2024.0755 · Cited by 11
Hartinger, R., Singh, K., Leverett, J. C., & Djabali, K. (2024) · Biomolecules · doi:10.3390/biom14101310 · Cited by 8
“The JAK-STAT and NF-κ B pathways play crucial roles in mediating inflammatory responses and are commonly upregulated during replicative senescence [20,46–48].”
BackgroundNiazi, S. K. (2025) · Life Sciences · doi:10.1016/j.lfs.2025.123904 · Cited by 8
Singh, I., & Singh, A. K. (2025) · Molecular Neurobiology · doi:10.1007/s12035-025-05504-1 · Cited by 10
Patel, H. A., Wang, J., Zinn, C. J., Learmonth, M., Bian, X., Jurk, D., Lerman, L. O., Wolfram, J., & Hickson, L. J. (2026) · Kidney International · doi:10.1016/j.kint.2025.10.019 · Cited by 8
Alamino, V. A., Onofrio, L. I., Acosta, C. D. V., Ferrero, P. V., Zacca, E. R., Cadile, I. I., Mussano, E. D., Onetti, L. B., Montes, C. L., Gruppi, A., et al. (2023) · European Journal of Immunology · doi:10.1002/eji.202250353 · Cited by 10
Lindenkamp, C., Plümers, R., Osterhage, M. R., Vanakker, O. M., Wynsberghe, J. V., Knabbe, C., & Hendig, D. (2023) · Biomedicines · doi:10.3390/biomedicines11102673 · Cited by 8
“As shown in the literature, blocking JAK/STAT3 signaling reduces inflammatory processes and cellular senescence in age-related processes and diseases [27,28].”
BackgroundParisi, S., Becciolini, A., Ditto, M. C., Gullo, A. L., Larosa, M., Palma, S., Olga, A., Reta, M., Paroli, M., Caccavale, R., et al. (2024) · Current Research in Pharmacology and Drug Discovery · doi:10.1016/j.crphar.2024.100178 · Cited by 8
“Despite all the limitations of the study, it is possible to explain this data as an effect of treatment with the JAK-i not only on the reduction of inflammatory phenomena directly mediated by rheumatoid arthritis, but also by immunosenescence (Xu et al., 2015).”
Conditioned medium of human mesenchymal stem cells affects stem cell senescence in osteoporosis
Liu, K., Sakai, K., Watanabe, J., Dong, J., Maruyama, H., Li, X., & Hibi, H. (2024) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2024.149858 · Cited by 8
IL‐6/STAT3‐mediated autophagy participates in the development of age‐related glomerulosclerosis
Zhu, X., Zhang, C., Shi, M., Li, H., Jiang, X., & Wang, L. (2021) · Journal of Biochemical and Molecular Toxicology · doi:10.1002/jbt.22698 · Cited by 8
Senotherapeutic Drugs: A New Avenue for Skincare?
Lee, B. P., & Harries, L. W. (2021) · Plastic & Reconstructive Surgery · doi:10.1097/prs.0000000000008782 · Cited by 9
p52 signaling promotes cellular senescence
Bernal, G. M., Wu, L., Voce, D. J., Weichselbaum, R. R., & Yamini, B. (2022) · Cell & Bioscience · doi:10.1186/s13578-022-00779-6 · Cited by 8
“5d), highlighting the senescence-inducing role of STAT3 [28].”
BackgroundJAK-STAT signaling mediates the senescence of cartilage-derived stem/progenitor cells
Ji, T., Chen, M., Sun, W., Zhang, X., Cai, H., Wang, Y., & Xu, H. (2022) · Journal of Molecular Histology · doi:10.1007/s10735-022-10086-6 · Cited by 8
“It has also been indicated that JAK-STAT signaling is involved in cellular senescence(Xu et al. 2015).”
BackgroundInci, N., Akyildiz, E. O., Bülbül, A., Turanlı, E. T., Akgün, E., Baykal, A. T., Çolak, F., & Bozaykut, P. (2022) · Biology · doi:10.3390/biology11091253 · Cited by 8
“That inflammation status is related to the SASP, which progressively changes tissue homeostasis and contributes to the aging-related phenotype [33].”
BackgroundCould senescence phenotypes strike the balance to promote tumor dormancy?
Chiu, F.-Y., Kvadas, R. M., Mheidly, Z., Shahbandi, A., & Jackson, J. G. (2023) · Cancer and Metastasis Reviews · doi:10.1007/s10555-023-10089-z · Cited by 8
Brinkley, T. E., Berger, M., Callahan, K. E., Fieo, R. A., Jennings, L. A., Morris, J. K., Wilkins, H., & Kritchevsky, S. B. (2018) · The Journals of Gerontology Series A · doi:10.1093/gerona/gly041 · Cited by 8
“In mice, clearance of senescent cells and suppression of the SASP through inducible transgenes, exercise, and/or an emerging class of drugs termed “senolytics” has been shown to extend parameters of healthspan and counteract age-associated syndromes and diseases, including frailty (23), vascular dysfunction (24), diab…”
Aging and immunity: the age-old tangoPreprint
Fernández-Maestre, I., Harris, A. S., & Amor, C. (2025) · Genes & Development · doi:10.1101/gad.352644.125 · Cited by 8
“…kinase (JAK) inhibitors, recognized for their anti-inflammatory properties and relative clinical success in treating myelo-proliferative neoplasms and autoinflammatory diseases, have shown senomorphic properties and alleviated frailty in aged mice, particularly in adipose tissue (Xu et al. 2015).”
Molecular and Inflammatory Etiologies of β-Cell Dysfunction in Type 1 Diabetes
Rostron, C. R., & Evans‐Molina, C. (2025) · Physiology · doi:10.1152/physiol.00008.2025 · Cited by 9
Battaglia-Vieni, A., Marchant, V., Tejedor-Santamaria, L., García-Caballero, C., Flores-Salguero, E., Ruiz-Torres, M. P., Rayego-Mateos, S., Sanz, A. B., Ortiz, A., & Ruiz-Ortega, M. (2025) · Pharmaceuticals · doi:10.3390/ph18060822 · Cited by 6
“IKK/NF-κ B and JAK inhibitors also suppress the SASP [60]; however, no protective effect has been described in acute AKI.”
Sigaud, R., Stefanski, A., Selt, F., Kocher, D., Usta, D., Picard, D. J., Büdenbender, I., Remke, M., Pfister, S. M., Jones, D., et al. (2025) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02279-8 · Cited by 9
Integrating Senescence and Oxidative Stress in Cardiac Disease
Yun, H. R., Singh, M. K., Han, S., Ranbhise, J. S., Ha, J., Kim, S. S., & Kang, I. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms262411917 · Cited by 8
“…conditions, including mammalian target of rapamycin complex 1 (mTORC1) inhibition with rapamycin [45], Janus kinase 1 and 2 (JAK1/2) blockade [46], bromodomain and extraterminal (BET)-bromodomain- containing protein 4 (BRD4) inhibition [47], p38-mitogen-activated protein kinase (MAPK) to…”
Cellular senescence as a therapeutic target for aging intervention
Bi, Y., & Ji, G. (2026) · Biomedical Journal · doi:10.1016/j.bj.2026.100948 · Cited by 9
“…muscle mass • May exacerbate sarcopenia • Osteoporosis model [127] • Preserved bone density; inhibited osteoclast activity • Naturally aged mice [117] • Reduced systemic inflammation and SASP markers; improved physical function • Increased susceptibility to infections • Metabolic syndrome [118]…”
Influential
Metadata
- Authors
- Xu, M., Tchkonia, T., Ding, H., Ogrodnik, M., Lubbers, E. R., Pirtskhalava, T., White, T. A., Johnson, K. O., Stout, M. B., Mezera, V., Giorgadze, N., Jensen, M. D., LeBrasseur, N. K., & Kirkland, J. L.
- Affiliations
- Mayo Clinic (US)
- Robert and Arlene Kogod Center on Aging,Mayo Clinic, Rochester, MN 55905;
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2015-11-02
- Volume
- 112
- Issue
- 46
- Pages
- E6301-10
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC4655580
- OpenAlex
- W1932046626
- Cited by
- 915
- References
- 68
- Citations by year
- 2026: 104 · 2025: 110 · 2024: 112 · 2023: 98 · 2022: 110 · 2021: 115 · 2020: 72 · 2019: 70 · 2018: 59 · 2017: 30 · 2016: 33 · 2015: 1
- FWCI
- 30.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Funders
- HHS | NIH | National Institute on Aging (AG041122, AG013925)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- JAK inhibition, cellular senescence, senescence-associated secretory phenotype, frailty, aging, age-related inflammation, adipose tissue, preadipocytes, macrophage migration, conditioned medium, endothelial cells, physical function, JAK inhibitors
- MeSH terms
- Adipose Tissue, Animals, Cell Movement, Extracellular Matrix, Humans, Macrophages, Signal Transduction, Cellular Senescence, Adipocytes, RNA, Small Interfering, Mice, Janus Kinases, Human Umbilical Vein Endothelial Cells
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