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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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“(iii) p16positive senescent cells were the main cause of increased IL-6 expression in the stromal vascular fraction of adipose tissue digests from older progeroid mice (21).”
BackgroundMethodInfluentialSelf-citationPrinciples of interleukin (IL)-6-type cytokine signalling and its regulation
HEINRICH, P. C., BEHRMANN, I., HAAN, S., HERMANNS, H. M., MÜLLER-NEWEN, G., & SCHAPER, F. (2003) · Biochemical Journal · doi:10.1042/bj20030407 · Cited by 3,272 · cited 1×
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Additional file 2 of Noncanonical Wnt5a signaling regulates tendon stem/progenitor cells senescence
Chen, M., Li, Y., Xiao, L., Dai, G., Lu, P., & Rui, Y. (2021) · Figshare · doi:10.6084/m9.figshare.16829714
Du, X., Peñalva, R. G., Little, K., Kissenpfennig, A., Chen, M., & Xu, H. (2021) · Figshare · doi:10.6084/m9.figshare.14059735
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Additional file 6 of Noncanonical Wnt5a signaling regulates tendon stem/progenitor cells senescence
Chen, M., Li, Y., Xiao, L., Dai, G., Lu, P., & Rui, Y. (2021) · Figshare · doi:10.6084/m9.figshare.16829726
Du, X., Peñalva, R. G., Little, K., Kissenpfennig, A., Chen, M., & Xu, H. (2021) · Figshare · doi:10.6084/m9.figshare.14059744
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Additional file 14 of Noncanonical Wnt5a signaling regulates tendon stem/progenitor cells senescence
Chen, M., Li, Y., Xiao, L., Dai, G., Lu, P., & Rui, Y. (2021) · Figshare · doi:10.6084/m9.figshare.16829708
Barber, A. J., del Genio, C. L., Swain, A. B., Pizzi, E. M., Watson, S. C., Tapiavala, V. N., Zanazzi, G. J., & Gaur, A. B. (2024) · Figshare · doi:10.6084/m9.figshare.26737980
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Du, X., Peñalva, R. G., Little, K., Kissenpfennig, A., Chen, M., & Xu, H. (2021) · Figshare · doi:10.6084/m9.figshare.14059747
Additional file 3 of Noncanonical Wnt5a signaling regulates tendon stem/progenitor cells senescence
Chen, M., Li, Y., Xiao, L., Dai, G., Lu, P., & Rui, Y. (2021) · Figshare · doi:10.6084/m9.figshare.16829717
Barber, A. J., del Genio, C. L., Swain, A. B., Pizzi, E. M., Watson, S. C., Tapiavala, V. N., Zanazzi, G. J., & Gaur, A. B. (2024) · Figshare · doi:10.6084/m9.figshare.26737977
Barber, A. J., del Genio, C. L., Swain, A. B., Pizzi, E. M., Watson, S. C., Tapiavala, V. N., Zanazzi, G. J., & Gaur, A. B. (2024) · Figshare · doi:10.6084/m9.figshare.26737971
Additional file 12 of Noncanonical Wnt5a signaling regulates tendon stem/progenitor cells senescence
Chen, M., Li, Y., Xiao, L., Dai, G., Lu, P., & Rui, Y. (2021) · Figshare · doi:10.6084/m9.figshare.16829702
Additional file 1 of Noncanonical Wnt5a signaling regulates tendon stem/progenitor cells senescence
Chen, M., Li, Y., Xiao, L., Dai, G., Lu, P., & Rui, Y. (2021) · Figshare · doi:10.6084/m9.figshare.16829711
Additional file 5 of Noncanonical Wnt5a signaling regulates tendon stem/progenitor cells senescence
Chen, M., Li, Y., Xiao, L., Dai, G., Lu, P., & Rui, Y. (2021) · Figshare · doi:10.6084/m9.figshare.16829723
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Additional file 9 of Noncanonical Wnt5a signaling regulates tendon stem/progenitor cells senescence
Chen, M., Li, Y., Xiao, L., Dai, G., Lu, P., & Rui, Y. (2021) · Figshare · doi:10.6084/m9.figshare.16829738
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Additional file 13 of Noncanonical Wnt5a signaling regulates tendon stem/progenitor cells senescence
Chen, M., Li, Y., Xiao, L., Dai, G., Lu, P., & Rui, Y. (2021) · Figshare · doi:10.6084/m9.figshare.16829705
Du, X., Peñalva, R. G., Little, K., Kissenpfennig, A., Chen, M., & Xu, H. (2021) · Figshare · doi:10.6084/m9.figshare.14059738
Lin, H., Chen, X., Pan, J., Ke, J., Zhang, A., Liu, Y., Wang, C., Chang, A. C. Y., & Gu, J. (2022) · Figshare · doi:10.6084/m9.figshare.20115872
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Additional file 11 of Noncanonical Wnt5a signaling regulates tendon stem/progenitor cells senescence
Chen, M., Li, Y., Xiao, L., Dai, G., Lu, P., & Rui, Y. (2021) · Figshare · doi:10.6084/m9.figshare.16829699
Barber, A. J., del Genio, C. L., Swain, A. B., Pizzi, E. M., Watson, S. C., Tapiavala, V. N., Zanazzi, G. J., & Gaur, A. B. (2024) · Figshare · doi:10.6084/m9.figshare.26737983
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Additional file 10 of Noncanonical Wnt5a signaling regulates tendon stem/progenitor cells senescence
Chen, M., Li, Y., Xiao, L., Dai, G., Lu, P., & Rui, Y. (2021) · Figshare · doi:10.6084/m9.figshare.16829696
Additional file 1 of Biomarkers of cellular senescence in idiopathic pulmonary fibrosis
Aversa, Z., Atkinson, E. J., Carmona, E. M., White, T. A., Heeren, A. A., Jachim, S. K., Zhang, X., Cummings, S. R., Chiarella, S. E., LIMPER, A. H., et al. (2023) · Figshare · doi:10.6084/m9.figshare.22624408
Self-citationBarber, A. J., del Genio, C. L., Swain, A. B., Pizzi, E. M., Watson, S. C., Tapiavala, V. N., Zanazzi, G. J., & Gaur, A. B. (2024) · Figshare · doi:10.6084/m9.figshare.26737956
Additional file 7 of Noncanonical Wnt5a signaling regulates tendon stem/progenitor cells senescence
Chen, M., Li, Y., Xiao, L., Dai, G., Lu, P., & Rui, Y. (2021) · Figshare · doi:10.6084/m9.figshare.16829729
Additional file 8 of Noncanonical Wnt5a signaling regulates tendon stem/progenitor cells senescence
Chen, M., Li, Y., Xiao, L., Dai, G., Lu, P., & Rui, Y. (2021) · Figshare · doi:10.6084/m9.figshare.16829735
Barber, A. J., del Genio, C. L., Swain, A. B., Pizzi, E. M., Watson, S. C., Tapiavala, V. N., Zanazzi, G. J., & Gaur, A. B. (2024) · Figshare · doi:10.6084/m9.figshare.26737968
Du, X., Peñalva, R. G., Little, K., Kissenpfennig, A., Chen, M., & Xu, H. (2021) · Figshare · doi:10.6084/m9.figshare.14059750
Lin, H., Chen, X., Pan, J., Ke, J., Zhang, A., Liu, Y., Wang, C., Chang, A. C. Y., & Gu, J. (2022) · Figshare · doi:10.6084/m9.figshare.20115857
Barber, A. J., del Genio, C. L., Swain, A. B., Pizzi, E. M., Watson, S. C., Tapiavala, V. N., Zanazzi, G. J., & Gaur, A. B. (2024) · Figshare · doi:10.6084/m9.figshare.26737986
Additional file 4 of Noncanonical Wnt5a signaling regulates tendon stem/progenitor cells senescence
Chen, M., Li, Y., Xiao, L., Dai, G., Lu, P., & Rui, Y. (2021) · Figshare · doi:10.6084/m9.figshare.16829720
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“Because p38 MAPK, ATM, and mTOR are central regulators of the SASP [21,22], these findings suggest that senescent macrophages activate pathways that promote SASP production.”
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“Janus kinases (JAK) inhibitors: Inhibition of JAK/signal transducer and activator of transcription protein signaling suppresses SASP cytokine production and inflammation[132].”
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“…senescent adipose tissue is considered a major contributor to age-associated systemic stress through SASP-related mechanisms (Tchkonia et al. 2010; Xu et al. 2015; Wang et al. 2022, 2025), suppression of adipose senescence-associated features may plausibly contribute to organism-level benefits.”
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Self-citationTissue turnover and rejuvenation through mechanics
Uchida, M., & Toyama, Y. (2026) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2026.1828482
“…activity, including rapamycin, which inhibits mTOR (mechanistic target of rapamycin)-driven SASP translation (Laberge et al., 2015); metformin, which suppresses NF-κ B activation (Moiseeva et al., 2013); and JAK (Janus kinase) inhibitors, which dampen SASP-driven inflammation (Xu et al., 2015).”
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“…with existing intervention evidence: rux-olitinib has been shown to potently suppress the SASP and reverse aging-related physical decline in vivo [38], positioning JAK inhibitors as a cornerstone class of seno-morphics [39]; targeting this pathway also attenuates tau pathology and cognitive…”
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
“JAK inhibitors (such as ruxolitinib) were the first to be demonstrated to effectively disrupt the autocrine positive feedback loop of the SASP, particularly that of IL-6, by inhibiting JAK/ STAT signal transduction [132].”
Targeting cellular senescence in dermatology: senolytic and senomorphic strategies
Haykal, D., Flament, F., Garibyan, L., Lee, S., Escot, J., Guéniche, A., & Kirkland, J. L. (2026) · GeroScience · doi:10.1007/s11357-026-02379-5
“• JAK inhibitors block SASP-mediated cytokine signaling and are already used in inflammatory dermatoses, potentially serving as indirect senom-orphics [33].”
Self-citationCellular senescence and senescence-associated secretory phenotypes
Yu, Z., Lai, H., XIANG, Y., & Xiao-Li, T. I. A. N. (2026) · Shengming kexue · doi:10.3724/cbls.2026095
Targeting the JAK-STAT signaling pathway ameliorates chemotherapy-induced skin aging
Li, J., Luo, Z., Zheng, Y., Wang, J., Cai, R., Chen, L., Shi, D., Zhang, D., Li, L., Chen, C., et al. (2026) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2026.117946
Yang, M., Jiang, X., Zhang, X., Deng, X., Chen, Y., Xie, W., Huang, Y., Lei, Y., Chen, J., Wang, Y., et al. (2026) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.6c02121
Wang, Y., Huang, Z., Tseng, Y., Ma, H., Chen, K., Pan, X., Ye, H., Cheng, T., Ge, J., Deng, J., et al. (2026) · Journal of Translational Medicine · doi:10.1186/s12967-026-08705-x
“Its inhibition can ameliorate the senescent phenotype, suppress SASP factor expression, and has been shown to extend healthspan, reduce tissue inflammation, and mitigate various senescence-associated pathologies [13–16].”
Song, Y., Zhang, R., Zhang, X., Wang, J., Chen, J., & Li, L. (2026) · Frontiers in Chemistry · doi:10.3389/fchem.2026.1861883
“Because the SASP is predominantly regulated by NF-κ B and JAK/STAT transcriptional networks, small-molecule interventions may attenuate the inflammatory microenvironment (Chien et al., 2011; Xu et al., 2015).”
Wang, Y., Luo, T., Li, C., Zhou, L., Lin, H., & Yang, M. (2026) · Experimental Eye Research · doi:10.1016/j.exer.2026.111189
Achudhan, D., Orme, J. J., Sharma, R., Komel, A., Khan, K. G., White, T. A., LeBrasseur, N. K., Khosla, S., Park, S. S., Pignolo, R. J., et al. (2026) · Journal of Bone and Mineral Research · doi:10.1093/jbmr/zjag122 · Cited by 1
Self-citationFuture perspectives: personalized medicine and senescence modulation in cardiovascular health
Nissar, I., Uppal, J., Gayaz, M., Chawla, A., Mohi-ud-din, R., Hussain, M. S., Mir, R. H., & Ahmad, A. (2026) · Elsevier eBooks · doi:10.1016/b978-0-443-45811-8.00008-8
Xue, Q., Yiganbaierdi, M., Wang, Y., Wang, M., Hou, X., Liang, R., Guo, Z., & Wang, Y. (2026) · In Silico Research in Biomedicine · doi:10.1016/j.insi.2026.100552
An ANGPTL8‐AKT2‐mTOR Axis Drives Adipose Senescence and Aging‐Related Functional Decline
He, Y., Pan, L., Ping, W., Meng, C., Meng, X., Guo, Y., Kan, R., Xiang, Y., Mao, B., Wang, S., et al. (2026) · Aging Cell · doi:10.1111/acel.70671
“Owing to its substantial mass, early susceptibility to cellular senescence, and robust secretory capacity, aging adipose tissue acts as a major source of circulating SASP factors that propagate inflammatory signals and exacerbate organismal aging (Islam et al. 2023; Xu et al. 2015).”
The senescence–immune axis as a target for combining immunotherapy and senotherapy
Saez‐Calazans, F., Grün, L. K., Stein, L. E., Barbé‐Tuana, F. M., & Filippi‐Chiela, E. C. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103309
Purkayastha, K., Roy, A., Bhattacharya, P., & Borah, A. (2026) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/j.bbagen.2026.130989
Chen, P., Wan, B., Yu, F., Zhang, Y., He, M., Wu, E., He, Y., Zhong, H., & Zhang, H. (2026) · Journal of Natural Medicines · doi:10.1007/s11418-026-02071-0
Etrouth, S., Zhu, Y., & Zhang, D. (2026) · Journal of Respiration · doi:10.3390/jor6030021
“The cells are attacked by monocytes, which produce cytotoxic molecules such as ROS, TNF-α , and nitric oxide, and lack CD47 (CD47 provides a “don’t eat me” signal) via TLR signaling [302,313].”
Remodeling the Immune Landscape: How Obesity-Induced SASPs Create a Pro-Tumorigenic Niche
El-Fattah, E. E. A., Ngai, G., Mooney, R., & Aboody, K. S. (2026) · Current Obesity Reports · doi:10.1007/s13679-026-00750-3
“…of obesity [79– 84 ], yet produce distinct but complementary proinflammatory outputs: senescent adipocytes survive and secrete SASP mediators [ 85 ], while PANoptotic cells die acutely and release a burst of IL-1β, IL-18, and DAMPs [ 86 ], as compared with other models, that further prime…”
Metabolically Active but Dysfunctional: The Impact of Senescent Cells and SASP
Xu, K., Viniak, S., Shah, P. V., Uddin, I. A., Alam, Z., & Khan, M. W. (2026) · Technology in Cancer Research & Treatment · doi:10.1177/15330338261481909
Li, F., Wang, Y., Wang, G., Chen, J., & Huang, S. (2026) · Aging Cell · doi:10.1111/acel.70658
“Similar effects are seen with glucocorticoids (corticosterone and cortisol), the JAK inhibitor ruxolitinib, NF-κB and p38 inhibitors, and pyrroloquinoline quinone (PQQ) (Laberge et al. 2012; Xu et al. 2015; Jiang et al. 2025).”
Maeda, T., Sato, H., NAKANO, Y., Kobayashi, H., Take, Y., Nisson, P. L., Cisneros, O., Rahmani, R., Jackson, B., Castro, J. C., et al. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103341
Lymphatic vascular aging and age-related bone loss: current status and future perspectives
Chudhary, M., Zhang, S., Docshin, P. M., Liu, J., Aripova, T., Zhou, J., Li, J., Malashicheva, A., & Liu, J. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1900206
“…by pharmacological evidence from de fi ned disease contexts: tocilizumab reduced bone resorption and increased femoral BMD in ACPA-positive rheumatoid arthritis, whereas JAK inhibition preserved bone integrity and restored lymphatic responsiveness in aged and progeria models (42, 49, 119, 123).”
Blocking PD-L2 prevents senescent cell accumulation and age-related dysfunction
Chaib, S., Prata, L. G. P. L., Suda, M., Sola, A., Mitchell, T. J., Anastasiadis, Z. P., Kunz, H., Nie, J., Victorelli, S. G., Flores, R. L., et al. (2026) · Cell Metabolism · doi:10.1016/j.cmet.2026.08.014
Self-citation
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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