The DOI matches its Crossref record; 216 of the 216 references it cites were found in a registry or an index.
Senescent cells: an emerging target for diseases of ageing
Open accessAbstract
Chronological age represents the single greatest risk factor for human disease. One plausible explanation for this correlation is that mechanisms that drive ageing might also promote age-related diseases. Cellular senescence, which is a permanent state of cell cycle arrest induced by cellular stress, has recently emerged as a fundamental ageing mechanism that also contributes to diseases of late life, including cancer, atherosclerosis and osteoarthritis. Therapeutic strategies that safely interfere with the detrimental effects of cellular senescence, such as the selective elimination of senescent cells (SNCs) or the disruption of the SNC secretome, are gaining significant attention, with several programmes now nearing human clinical studies.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source doesn’t support the claim as written.
In the citing paper
“In cancer, the SASP can frequently promote therapy resistance and recurrence [34].”
From The role of cellular senescence and SASP in tumour microenvironment (2023) · cites this paper as [34]
Checked by a reasoning model — may be wrong.
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
“While senescence has beneficial functions (such as tumor suppression), senescent cells accumulate in most tissues with age, and they are important components of the overall aging process62.”
From The role of retrotransposable elements in ageing and age-associated diseases (2021) · cites this paper as [62]
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
“Several senolytic drugs, such as ABT‐737, BET inhibitors and dasatinib plus quercetin, can selectively induce cell death in senescent cells and effectively improve some symptoms of age‐related disease, including cancer, by attenuating SASP factor production.81”
From Cellular senescence and senescence-associated secretory phenotype via the cGAS-STING signaling pathway in cancer (2020) · cites this paper as [81]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The literature is becoming inundated with evidence that senescent cells accumulate in a variety of age-associated diseases13.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [13]
In the citing paper
“In particular, this failsafe cellular senescence reportedly occurs in response to (1) potentially carcinogenic events including oncogene activation or oncosuppressor gene inactivation; and (2) several sublethal cellular insults, including telomere shortening, DNA damage, mitochondrial dysfunction, defective/stalled DNA replication and epigenetic, lysosomal, mechanical, metabolic, mitotic, ox”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [958]
In the citing paper
“Genetic and pharmacological strategies have demonstrated the benefits of eliminating senescent cells in the context of aging and disease 10,12,51.”
From Cardiac glycosides are broad-spectrum senolytics (2019) · cites this paper as [51]
In the citing paper
“Organismal aging and age-related diseases promote an accumulation of senescent cells in a variety of tissues in both humans and mice (8).”
From Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives (2018) · cites this paper as [8]
In the citing paper
“Senescent cells are more than simple bystanders, as multiple molecules involved in the SASP act as promoters of atherosclerosis and are biomarkers of CVD risk.23”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [23]
In the citing paper
“Small molecules that can selectively kill SCs, termed senolytics, have the potential to prevent and treat a growing number of age-related diseases and extend healthspan2–4.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [2]
In the citing paper
“SCs accumulate with age and as a result of the exposure to a variety of stressors including radiation.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [2]
In the citing paper
“By contrast, almost all the targeted senolytics are repurposed anticancer agents except the FOXO4-p53 interfering peptide2–4.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [2]
In the citing paper
“They play a causal role in many age-related diseases (such as neurodegenerative and cardiovascular diseases, osteoarthritis, and cancer) via expression of the senescence-associated secretory phenotype (SASP) to secret various inflammatory mediators and proteases1–7.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [2]
In the citing paper
“Our studies also confirm some of the previous observations that SCs from different cellular origins and tissues show variable sensitivities to different senolytic agents2–5.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [2]
In the citing paper
“This observation is in agreement with the suggestion that different SCs can use different anti-apoptotic pathways (SCAPs) to resist apoptosis2–5.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [2]
In the citing paper
“Cell senescence occurs throughout the lifespan but plays a larger role with aging and is postulated to contribute to many diseases of aging including vascular disease, arthritis, and neurodegeneration. 38”
From Alzheimer’s disease drug development pipeline: 2021 (2021) · cites this paper as [38]
In the citing paper
“Excessive accumulation of senescent cells in numerous tissues leads to multiple chronic diseases, tissue dysfunction, age-related diseases and organ ageing.”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [14]
In the citing paper
“However, excessive accumulation of senescent cells causally shortens the healthy lifespan [11] and drives organ ageing [12], age-related organ deterioration/disorders [13,14], tissue dysfunction and chronic diseases, including cardiovascular diseases (CVDs) [15,16], cancer [2], neurodegenerative diseases [17,18] and osteoarthritis [19].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [14]
In the citing paper
“However, the senolytic drugs identified to date were not discovered by a truly unbiased high-throughput screening (HTS) method, and thus appear to have limitations in clinical applications15,17–19.”
From A BET family protein degrader provokes senolysis by targeting NHEJ and autophagy in senescent cells (2020) · cites this paper as [15]
In the citing paper
“the combination of dasatinib and quercetin (D + Q), another previously reported senolytic drug20, apparently exhibited remarkable cell-type specificity15”
From A BET family protein degrader provokes senolysis by targeting NHEJ and autophagy in senescent cells (2020) · cites this paper as [15]
In the citing paper
“in a phase II study of ABT263 (a specific inhibitor of the anti-apoptotic proteins BCL2 and BCL-xL)19 for the treatment of advanced and recurrent small-cell lung carcinoma patients, transient thrombocytopenia and neutropenia were reported as side-effects15.”
From A BET family protein degrader provokes senolysis by targeting NHEJ and autophagy in senescent cells (2020) · cites this paper as [15]
In the citing paper
“Cellular senescence impairs the ability of tissue regeneration and drives chronic low-grade inflammation, which exacerbates the aging process.5,6”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [6]
In the citing paper
“Cellular senescence impairs the ability of tissue regeneration and drives chronic low-grade inflammation, which exacerbates the aging process.5,6”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [6]
In the citing paper
“These studies demonstrated that senescence is one of the major drivers of aging and that clearing senescent cells is a promising approach to treat age-related diseases and improve physical function.6,10”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [6]
In the citing paper
“However, senolytic drugs have significant limitations in killing senescent cells in terms of specificity and broad-spectrum activity because of the dynamic and highly heterogeneous nature of the senescence program, which leads to the varying sensitivity of different types of senescent cells to current senolytic drugs.6,16,17”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [6]
In the citing paper
“SASP contributes to local and systemic low-grade inflammation during aging, to age-related degenerative phenotypes, and to impairment of physical function.5,6,43”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [6]
In the citing paper
“Senescent cells produce a distinct inflammatory secretome and have been found to accumulate with age and in many diseases; potentially contributing to pathology [17–21].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [17]
In the citing paper
“Senescent cells produce a distinct inflammatory secretome and have been found to accumulate with age and in many diseases; potentially contributing to pathology [17–21].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [17]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
The serial cultivation of human diploid cell strains
Hayflick, L., & Moorhead, P. S. (1961) · Experimental Cell Research · doi:10.1016/0014-4827(61)90192-6 · Cited by 8,508
A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
Dimri, G. P., Lee, X., Basile, G., Acosta, M., Scott, G., Roskelley, C., Medrano, E. E., Linskens, M., Rubelj, I., & Pereira-Smith, O. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.20.9363 · Cited by 7,477
The limited in vitro lifetime of human diploid cell strains
Hayflick, L. (1965) · Experimental Cell Research · doi:10.1016/0014-4827(65)90211-9 · Cited by 5,876
Lawrence, R. C., Felson, D. T., Helmick, C. G., Arnold, L. M., Choi, H. K., Deyo, R. A., Gabriel, S. E., Hirsch, R., Hochberg, M. C., Hunder, G. G., et al. (2007) · Arthritis & Rheumatism · doi:10.1002/art.23176 · Cited by 5,599
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218
Cellular senescence: when bad things happen to good cells
Campisi, J., & d'Adda di Fagagna, F. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2233 · Cited by 4,441
Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders
Baker, D. J., Wijshake, T., Tchkonia, T., LeBrasseur, N. K., Childs, B. G., van de Sluis, B., Kirkland, J. L., & van Deursen, J. M. (2011) · Nature · doi:10.1038/nature10600 · Cited by 3,670
Self-citationA new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4.
Serrano, M., Hannon, G. J., & Beach, D. (1993) · Nature · doi:10.1038/366704a0 · Cited by 3,650
Chronic Health Conditions in Adult Survivors of Childhood Cancer
Oeffinger, K. C., Mertens, A. C., Sklar, C. A., Kawashima, T. I., Hudson, M. M., Meadows, A. T., Friedman, D. L., Marina, N. M., Hobbie, W. L., Kadan‐Lottick, N. S., et al. (2006) · New England Journal of Medicine · doi:10.1056/nejmsa060185 · Cited by 3,597
Aging, Cellular Senescence, and Cancer
Campisi, J. (2013) · Annual Review of Physiology · doi:10.1146/annurev-physiol-030212-183653 · Cited by 2,954
Research works printed but not linked: 1
- Weismann, A. Collected Essays upon Heredity and Kindred Biological Problems (ed. Poulton, E. B.) (Clarendon, 1881).
Cited by
Sorted by citations
Items 801–900 of 1,000
A β-galactosidase kiss of death for senescent cells
Liu, X., Belmonte, J. C. I., Zhang, W., & Liu, G. (2020) · Cell Research · doi:10.1038/s41422-020-0325-6 · Cited by 8
Emerging injectable therapies for osteoarthritis
Sewell, J., & Östör, A. J. K. (2022) · Expert Opinion on Emerging Drugs · doi:10.1080/14728214.2022.2125506 · Cited by 8
An evaluation of the role of miR-361-5p in senescence and systemic ageing
Manni, E., Jeffery, N. M., Chambers, D., Slade, L., Etheridge, T., & Harries, L. W. (2023) · Experimental Gerontology · doi:10.1016/j.exger.2023.112127 · Cited by 9
Advances in biomarkers and diagnostic significance of organ aging
Chen, Y., Li, J., Liu, X., Geng, Z., Xu, K., & Su, J. (2023) · Fundamental Research · doi:10.1016/j.fmre.2023.03.009 · Cited by 9
Zhang, Y., Wang, T., Song, Y., Chen, M., Hou, B., Yao, B., Ma, K., Song, Y., Wang, S., Zhang, D., et al. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e27646 · Cited by 8
El-Baz, F. K., Saleh, D. O., Jaleel, G. A. A., & Hussein, R. A. (2020) · Advances in Pharmacological and Pharmaceutical Sciences · doi:10.1155/2020/3797218 · Cited by 8
Senescent Cell-Secreted Netrin-1 Modulates Aging-Related Disorders by Recruiting Sympathetic Fibers
Yu, A. Q., Wang, J., Zhou, X. J., Chen, K. Y., Cao, Y. D., Wang, Z. X., & Mao, Z. B. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.507140 · Cited by 9
Therapeutic effects and perspective of stem cell extracellular vesicles in aging and cancer
Liu, Y., Cheng, Y., Wang, S., Su, Y., Liu, Y., Li, C., Jin, L., Wan, Q., Sang, X., & Wang, Z. (2020) · Journal of Cellular Physiology · doi:10.1002/jcp.30212 · Cited by 9
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
Ayurvedic Rasayana Therapy: A Rational Understanding Necessary for Mass Benefits
Rastogi, S., Lakhotia, S. C., & Singh, R. H. (2018) · Springer eBooks · doi:10.1007/978-981-13-2062-0_6 · Cited by 8
Zhang, Y., Guo, P., Xiang, W., Liu, Q., Liu, X., Ma, N., Zhou, S., He, H., Wlaschek, M., Scharffetter‐Kochanek, K., et al. (2020) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2020/5367102 · Cited by 8
Resolvin D1 suppresses macrophage senescence and splenic fibrosis in aged mice
Groenen, A. G., Lipscomb, M., Ramos, R. B., Sadhu, S., Bazioti, V., Fredman, G., & Westerterp, M. (2024) · Prostaglandins Leukotrienes and Essential Fatty Acids · doi:10.1016/j.plefa.2024.102634 · Cited by 7
Immune therapeutic strategies for the senescent tumor microenvironment
Yasuda, T., & Wang, Y. (2024) · British Journal of Cancer · doi:10.1038/s41416-024-02865-7 · Cited by 10
Komleva, Y. K., Shpiliukova, K. A., Bondar, N., Salmina, A. B., Хилажева, Е. Д., Illarioshkin, S. N., & Пирадов, М. А. (2025) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2025.1562453 · Cited by 9
Giroud, J., Delvaux, P., Carlier, L., de Schutter, C., Martin, N., Rouget, R., Bolouki, A., Glas, V. D., Bouriez, I., Bourdoux, F., et al. (2025) · Aging Cell · doi:10.1111/acel.70024 · Cited by 7
Microbiota-derived corisin accelerates kidney fibrosis by promoting cellular aging
Yasuma, T., Fujimoto, H., D’Alessandro‐Gabazza, C. N., Toda, M., Uemura, M., Nishihama, K., Takeshita, A., D’Alessandro, V. F., Okano, T., Okano, Y., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-61847-2 · Cited by 9
Deng, Y., He, X., Peng, J., Pan, Y., Luo, Y., Ruan, Y., Hou, J., Jiang, B., Li, X., Liang, X., et al. (2025) · Cell Death and Disease · doi:10.1038/s41419-025-08007-y · Cited by 8
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
Ferreira, D., Chmiela, T., Eriksdotter, M., Jack, C. R., Kalpouzos, G., Marseglia, A., Mecocci, P., Nordberg, A. K., Religa, D., & Westman, E. (2026) · Journal of Internal Medicine · doi:10.1111/joim.70096 · Cited by 7
Fernandes, S. E., Alakesh, A., Rajmani, R. S., Jhunjhunwala, S., & Saini, D. K. (2021) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2021.119063 · Cited by 7
Luo, C., Nakagawa, M., Yoichi, S. U. M. I., Matsushima, Y., Uemura, M., Honda, Y., & Matsumoto, N. (2024) · Dental Materials Journal · doi:10.4012/dmj.2023-262 · Cited by 7
Senolysis of gemcitabine‐induced senescent human pancreatic cancer cells
Hoque, M. M., Iida, Y., Kotani, H., & Harada, M. (2024) · Cancer Reports · doi:10.1002/cnr2.2075 · Cited by 7
Ji, J., Zhang, B., Zheng, J., Zhang, X., Hu, X., Zhu, H., Wang, P., & Lan, Z. (2025) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2025.119883 · Cited by 7
Elimination of senescent cells prevents neurodegeneration in mice
Penney, J., & Tsai, L. (2018) · Nature · doi:10.1038/d41586-018-06677-7 · Cited by 7
Ray, M., Singh, G., & Lakhotia, S. C. (2019) · Gene Expression Patterns · doi:10.1016/j.gep.2019.05.002 · Cited by 7
Suzuki, K., Kawamura, K., Ujiie, R., Nakayama, T., & Mitsutake, N. (2022) · Mutation Research/Genetic Toxicology and Environmental Mutagenesis · doi:10.1016/j.mrgentox.2022.503448 · Cited by 8
ML216 Prevents DNA Damage-Induced Senescence by Modulating DBC1–BLM Interaction
Cui, F., Han, X., Zhang, X., Wang, S., Liang, N., Tan, Q., Sha, W., & Li, J. (2022) · Cells · doi:10.3390/cells12010145 · Cited by 7
Mazzucca, C. B., Cappellano, G., & Chiocchetti, A. (2023) · CNS & Neurological Disorders - Drug Targets · doi:10.2174/1871527322666230502123255 · Cited by 7
Zeng, T., Jiang, S., Wang, Y., Sun, G., Cao, J., Hu, D., Wang, G., Liang, X., Ding, J., & Du, J. (2023) · Cell Cycle · doi:10.1080/15384101.2023.2213926 · Cited by 8
Loss of fragile WWOX gene leads to senescence escape and genome instability
Cheng, H., Huang, P.-H., Lai, F., Jan, M., Chen, Y., Chen, S.-Y., Chen, W., Hsu, C., Huang, W., & Hsu, L. (2023) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-023-04950-1 · Cited by 8
Yan, J., Yao, L., Tan, Y. H. V., & Wang, Y. (2023) · Aging · doi:10.18632/aging.205024 · Cited by 7
Cibler les cellules sénescentes
Tachikart, Y., Malaise, O., Constantinides, M., Jørgensen, C., & Brondello, J. (2018) · médecine/sciences · doi:10.1051/medsci/20183406014 · Cited by 8
Nuriliani, A., Nakahata, Y., Ahmed, R., Khaidizar, F. D., Matsui, T., & Bessho, Y. (2020) · Genes to Cells · doi:10.1111/gtc.12794 · Cited by 7
Targeting senescent cells and tumor therapy (Review)
Wang, Z., Gao, J., Liu, H., Ohno, Y., & Xu, C. (2020) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2020.4705 · Cited by 8
Ye, L., Huang, J., Xiang, X., Song, S., Huang, G., Ruan, Y., & Wu, S. (2021) · Steroids · doi:10.1016/j.steroids.2021.108829 · Cited by 7
Tryfonos, A., Mills, J. D., GREEN, D. J., Wagenmakers, A. J. M., Dawson, E. A., & Cocks, M. S. (2022) · European Journal of Applied Physiology · doi:10.1007/s00421-022-05040-z · Cited by 7
Breathe it in – Spotlight on senescence and regeneration in the lung
Majewska, J., & Krizhanovsky, V. (2021) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2021.111550 · Cited by 7
Xia, Y., Li, J., Wang, L., Luo, X., Xie, Y., & Liu, Y. (2022) · Angewandte Chemie · doi:10.1002/ange.202115764 · Cited by 7
Biologic Augmentation of Rotator Cuff Repair: Current Concepts Review
Uyeki, C. L., Ford, B. T., Shuman, M. E., Hawthorne, B. C., Wellington, I. J., & Mazzocca, A. D. (2024) · Orthopedics · doi:10.3928/01477447-20241028-01 · Cited by 6
Zhang, Z., He, T., Gu, H., Zhao, Y., Tang, S., Han, K., Hu, Y., Wang, H., & Yu, H. (2024) · BMC Molecular and Cell Biology · doi:10.1186/s12860-024-00519-3 · Cited by 6
Feng, Y., Zhu, Z., Zhao, S., Jiang, X., Zhang, W., & Xu, Z. (2025) · Bioconjugate Chemistry · doi:10.1021/acs.bioconjchem.5c00109 · Cited by 6
Wang, C., Chen, D., Yin, Y., Liu, X., Liu, Y., Li, X., Kong, C., & Zhao, Q. (2025) · Renal Failure · doi:10.1080/0886022x.2025.2511275 · Cited by 6
Albarrati, A., & Gale, N. (2025) · Current Issues in Molecular Biology · doi:10.3390/cimb47070561 · Cited by 6
Elaidic acid drives cellular senescence and inflammation via lipid raft-mediated IL-1R signaling
Kojima, R., Hirata, Y., Ashida, R., Takahashi, M., Matsui, R., Hama, K., Watanabe, A., Takita, R., Sato, E., Abe, T., et al. (2025) · iScience · doi:10.1016/j.isci.2025.113305 · Cited by 6
NR4A1 Acts as a Nutrient Sensor That Inhibits the Effects of Aging
Safe, S. H. (2025) · Nutrients · doi:10.3390/nu17162709 · Cited by 7
Luo, J., Tian, Z., Yuan, W., Peng, X., Zhou, H., Shen, Q. W., Luo, Y., Guo, Y., Shi, Z., Jiang, X., et al. (2025) · Food Bioscience · doi:10.1016/j.fbio.2025.106582 · Cited by 6
Rovira, I. I., Biragyn, A., Brown, L. L., Galis, Z. S., Klauzińska, M., Kotliarova, S. E., Simmons, J. M., Wali, A., Xi, D., Yarden, R. I., et al. (2025) · Frontiers in Public Health · doi:10.3389/fpubh.2025.1462217 · Cited by 7
Targeting senescent cell clearance: An approach to delay aging and age-associated disorders
Qiu, Z., Jia, J., Zou, H., Ao, Y., Liu, B., & Wang, Z. (2021) · Translational Medicine of Aging · doi:10.1016/j.tma.2020.12.001 · Cited by 6
He, Y., Zheng, G., & Zhou, D. (2020) · Healthy ageing and longevity · doi:10.1007/978-3-030-44903-2_1 · Cited by 6
Cross-Tissue Analysis Using Machine Learning to Identify Novel Biomarkers for Knee Osteoarthritis
Zhao, Y., Xia, Y., Kuang, G., Cao, J.-H., Shen, F., & Ming-shuang, Z. (2022) · Computational and Mathematical Methods in Medicine · doi:10.1155/2022/9043300 · Cited by 6
Heo, S.-J., Park, S., & Jee, Y. (2023) · Archives of Gerontology and Geriatrics · doi:10.1016/j.archger.2023.105273 · Cited by 6
Henze, L., Walter, U., Escobar, H. M., Junghanß, C., Jaster, R., Köhling, R., Lange, F., Salehzadeh‐Yazdi, A., Wolkenhauer, O., Hamed, M., et al. (2020) · BMJ Open · doi:10.1136/bmjopen-2020-039560 · Cited by 6
Calvo, L., Cheng, S., Skulimowski, M., Clément, I., Portelance, L., Zhan, Y., Carmona, E., Lafontaine, J., de Ladurantaye, M., Rahimi, K., et al. (2018) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/425199 · Cited by 6
Pharmacological frontiers in senescence: Transforming senescence with drug repurposing
Shahzadi, A., Özyazgan, S., & Çakatay, U. (2025) · Advances in pharmacology · doi:10.1016/bs.apha.2025.02.010 · Cited by 5
Li, J., Rong, M., Liu, C., & Lu, L. (2025) · ACS Nano · doi:10.1021/acsnano.5c05124 · Cited by 5
Shahzaib, M., Aprile, D., Squillaro, T., Alessio, N., Peluso, G., Bernardo, G. D., & Galderisi, U. (2025) · Ageing Research Reviews · doi:10.1016/j.arr.2025.102916 · Cited by 6
Enomoto, S., Hur, Y. H., Solodova, T., Neumann, J., Cerione, R. A., & Antonyak, M. A. (2025) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2025.110821 · Cited by 5
The drug discovery and therapeutic nano-strategies targeting cellular senescence
Wang, Y., Liu, M., Chen, X., Wang, S., Li, J., Sun, Y., Zheng, X., Zhang, J.-X., & Li, H. (2025) · Materials Today Bio · doi:10.1016/j.mtbio.2025.102480 · Cited by 6
Antonangeli, F., Arcuri, E., & Santoni, A. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1694567 · Cited by 5
The Role of Oligodendrocytes in Alzheimer’s Disease Pathogenesis and Therapy
Guo, S., Yu, X., & Zhang, H. (2025) · Neuroglia · doi:10.3390/neuroglia6040046 · Cited by 5
Wang, Z., Chen, X., Xu, Y., Guo, X., Liu, X., Dai, X., Lü, J., Qi, J., Zheng, T., Zhang, L., et al. (2025) · ACS Nano · doi:10.1021/acsnano.5c17402 · Cited by 5
Qiao, W., Huang, M. N., Chen, L., Goltzman, D., & Miao, D. (2025) · Frontiers in Bioscience-Landmark · doi:10.31083/fbl46123 · Cited by 5
DEL‐1 is an Endogenous Senolytic Protein that Inhibits Senescence‐Associated Bone Loss
Lim, J., Sirisereephap, K., Wang, H., Trimaglio, G., Chung, K., Korostoff, J. M., Kajikawa, T., Li, X., Surboyo, M. D. C., Maekawa, T., et al. (2026) · Advanced Science · doi:10.1002/advs.202509263 · Cited by 5
S100A8/A9 as a central hub in inflammaging: Cross-system mechanisms
Wang, S., Ni, Y., Feng, J., Zhang, W., Zhou, M., & Zhao, C. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103108 · Cited by 5
Cantero‐Fortiz, Y., Butler, C., Montalbán, X., & Boada, M. (2026) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2026.1805691 · Cited by 6
Senescence as a therapeutic target
Meyer, K. R., Lopez-Dominguez, J. A., Maus, M., Kovatcheva, M., & Serrano, M. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-822514-1.00014-6 · Cited by 5
Zhu, Y., Tazearslan, C., Rosenfeld, M. G., Fiser, A., & Suh, Y. (2023) · Aging Cell · doi:10.1111/acel.13908 · Cited by 5
Cellular senescence and nanoparticle-based therapies: Current developments and perspectives
Henschke, A., Mielcarek, A., Grześkowiak, B. F., Perrigue, P. M., Jaskot, K., Coy, E. L., & Moya, S. E. (2024) · Nanotechnology Reviews · doi:10.1515/ntrev-2023-0211 · Cited by 6
Kat7 accelerates osteoarthritis disease progression through the TLR4/NF-κB signaling pathway
Liu, Z., Qiu, L., Zhang, Y., Zhao, G., Sun, X., & Luo, W. (2025) · Journal of Molecular Medicine · doi:10.1007/s00109-025-02519-y · Cited by 5
Lissa, D., Joruiz, S. M., Dranchak, P. K., Ungerleider, K., Yamada, L., Horikawa, I., Oliphant, E. N., Manubag, R., von Muhlinen, N., Beck, J. A., et al. (2025) · ACS Pharmacology & Translational Science · doi:10.1021/acsptsci.5c00186 · Cited by 5
Xu, Y., Han, T., Wu, Y., Liu, H., Hou, K., An, Z., Li, Y., Zhu, C., Wang, S., & Wei, J. (2025) · Neuroscience Bulletin · doi:10.1007/s12264-025-01505-1 · Cited by 5
Ma, Y., Cao, C., Zhao, M., Liu, X., Cheng, F., & Wang, J. (2021) · Journal of Molecular Neuroscience · doi:10.1007/s12031-021-01874-y · Cited by 5
Circular RNAs: Regulators of endothelial cell dysfunction in atherosclerosis
Jin, T., Wang, H., Liu, Y., & Wang, H. (2024) · Journal of Molecular Medicine · doi:10.1007/s00109-023-02413-5 · Cited by 5
Uncovering cellular senescence as a therapeutic target in NF2-related vestibular schwannoma
Franco-Caspueñas, S., García‐Montoya, C., Contreras, J., Lassaletta, L., Varela‐Nieto, I., & Jimenez-Lara, A. M. (2024) · Hearing Research · doi:10.1016/j.heares.2024.109165 · Cited by 5
Zhang, K., Yin, Q., Ma, Y. F., Cao, M., Li, L., Jin, X. M., & Leng, J. (2025) · Human Vaccines & Immunotherapeutics · doi:10.1080/21645515.2025.2479229 · Cited by 5
Pathophysiology and genetics in craniopharyngioma
Apps, J. R., & Martı́nez-Barberá, J. P. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-819949-7.00020-2 · Cited by 5
Mitoribosomal Deregulation Drives Senescence via TPP1-Mediated Telomere Deprotection
Min, S., Kwon, S. M., Hong, J., Lee, Y., Park, T. J., Lim, S. B., & Yoon, G. (2022) · Cells · doi:10.3390/cells11132079 · Cited by 7
RagC GTPase regulates mTOR to promote chemoresistance in senescence-like HepG2 cells
Jiang, W., Ou, Z., Zhu, Q., Yao, Y., & Zai, H. (2022) · Frontiers in Physiology · doi:10.3389/fphys.2022.949737 · Cited by 5
Therapeutic Potential of a Senolytic Approach in a Murine Model of Chronic GVHD
Raman, D., Chêne, C., Nicco, C., Jeljeli, M. M., Eu, J. Q., Clement, M., Batteux, F., & Pervaiz, S. (2023) · Biology · doi:10.3390/biology12050647 · Cited by 5
Dai, G., Li, M., He, X., & Quan, N. (2023) · Current Problems in Cardiology · doi:10.1016/j.cpcardiol.2023.101910 · Cited by 5
Hautalterung – zelluläre Seneszenz
Scharffetter‐Kochanek, K., Wang, Y., Makrantonaki, E., Crișan, D., Wlaschek, M., Geiger, H., & Maity, P. (2023) · Die Dermatologie · doi:10.1007/s00105-023-05201-x · Cited by 5
Restoration of miR-223-3p expression in aged mouse uteri with Samul-tang administration
Kim, J., & You, S. (2022) · Integrative Medicine Research · doi:10.1016/j.imr.2022.100835 · Cited by 5
Establishment of a cell senescence related prognostic model for predicting prognosis in glioblastoma
Li, H., Wang, Z., Sun, C., & Li, S. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.1034794 · Cited by 6
Franceschi, C., Capri, M., Garagnani, P., Ostan, R., Santoro, A., Monti, D., & Salvioli, S. (2019) · Springer eBooks · doi:10.1007/978-3-319-99375-1_45 · Cited by 6
La sénescence en passe d’être vaincue ?
Jordan, B. (2018) · médecine/sciences · doi:10.1051/medsci/2018222 · Cited by 5
Procyanidin C1 is a natural agent with senolytic activity against aging and age-related diseasesPreprint
Xu, Q., Fu, Q., Li, Z., Liu, H., Wang, Y., Lin, X., He, R., Zhang, X., Campisi, J., Kirkland, J. L., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.04.14.439765 · Cited by 5
Chi, H., Ma, L., Zeng, F., Wang, X., Peng, P., Bai, X., Zhang, T., Yin, W., Yu, Y., Yang, L., et al. (2025) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.66.2.15 · Cited by 4
Overexpression of βTrCP1 elicits cell death in cisplatin-induced senescent cells
Belmonte‐Fernández, A., Herrero‐Ruiz, J., Limón‐Mortés, M. C., Sáez, C., Japón, M. Á., Mora‐Santos, M., & Romero, F. (2025) · Cell Death and Disease · doi:10.1038/s41419-025-07556-6 · Cited by 4
Dai, D., Gao, L.-B., Pan, Y., Chen, C., Ma, K., Zhang, H., Wu, S., Qi, G., & Wang, J. (2025) · Poultry Science · doi:10.1016/j.psj.2025.105258 · Cited by 4
Wang, F., Zhou, L., Zhong, Y., Cai, Y., Meng, X., Chen, M., Mao, R., Xiao, X., Yi, C., Guo, Y., et al. (2025) · MedComm · doi:10.1002/mco2.70205 · Cited by 4
Chen, Z. (2025) · American journal of clinical and experimental immunology. · doi:10.62347/xrgr9217 · Cited by 4
Neurodegeneration and aging: pathophysiology, diagnosis, and therapeutic targets
Thakur, A., Sharma, R., Sharma, R. R., & Devi, A. (2025) · Inflammopharmacology · doi:10.1007/s10787-025-01991-9 · Cited by 4
Mechanisms of aging in the cardiovascular system: challenges and opportunities
Zhao, X., Yang, X., Lin, Y., Lei, R., Ding, W., He, X.-Y., Cao, Y. J., Zhang, D., Liu, P., Liang, M., et al. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1635736 · Cited by 4
Jin, C., Xu, X., Yao, N., Zhang, H., Chen, C. F., Zeng, L., Liu, Z., Lei, L., Cui, S., Wen, C., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-67364-6 · Cited by 4
Chen, L., Li, J., Wang, S., Ren, R., Xiong, W., Gan, X., Kang, H., Wen, Y., Li, J., & He, L. (2026) · International Immunopharmacology · doi:10.1016/j.intimp.2026.116450 · Cited by 4
Gaspary, J. F. P., Lopes, L. F. D., Gaspary, F. P., Lopes, E. G., Edgar, A. L., Camara, E. P., & Camara, A. G. (2026) · Frontiers in Medicine · doi:10.3389/fmed.2026.1824897 · Cited by 4
Laboratory Techniques in Cellular and Molecular Medicine
Ed., J. S., Janošťáková, A., Das, V., Kudlová, N., Stránská, J., Buriánová, R., Kotulová, J., Schadich, E., Ondra, M., Kubíčková, A., et al. (2022) · doi:10.5507/lf.22.24460499 · Cited by 5
Extracellular Vesicles and Cellular Ageing
Romero-García, N., Mas‐Bargues, C., Huete-Acevedo, J., & Borrás, C. (2023) · Sub-cellular biochemistry/Subcellular biochemistry · doi:10.1007/978-3-031-21410-3_11 · Cited by 5
Inactivation of Myostatin Delays Senescence via TREX1-SASP in Bovine Skeletal Muscle Cells
Yang, M., Gao, L., Gao, Y., Hao, Z., Zhou, X., Su, G., Bai, C., Wei, Z., Liu, X., Yang, L., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25105277 · Cited by 4
A Youthful Touch: Reversal of Aging Hallmarks by Cell Reprogramming
Miliotou, E., & de Lázaro, I. (2024) · Cells Tissues Organs · doi:10.1159/000539415 · Cited by 4
Metadata
- Authors
- Childs, B. G., Gluscevic, M., Baker, D. J., Laberge, R.-M., Marquess, D., Dananberg, J., & van Deursen, J. M.
- Affiliations
- Mayo Clinic (US)
- Unity Biotechnology (United States) (US)
- Venue
- Nature Reviews Drug Discovery
- Published
- 2017-07-21
- Volume
- 16
- Issue
- 10
- Pages
- 718-735
- ISSN
- 1474-1776 (ISSN-L)
- 1474-1784
- PMC
- PMC5942225
- OpenAlex
- W2739438570
- Cited by
- 1,284
- References
- 216
- Citations by year
- 2026: 146 · 2025: 157 · 2024: 166 · 2023: 162 · 2022: 149 · 2021: 168 · 2020: 146 · 2019: 108 · 2018: 73 · 2017: 8
- FWCI
- 11.24
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Drug Discovery (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Funders
- National Institute on Aging (T32AG049672)
- National Cancer Institute (R01CA168709, R01CA096985)
- 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
- cellular senescence, senescent cells, aging, age-related diseases, cancer, atherosclerosis, osteoarthritis, senolytics, senescence-associated secretory phenotype, cell cycle arrest, cellular stress, senolytic therapy
- MeSH terms
- Aging, Animals, Humans, Neoplasms, Cellular Senescence, Cell Proliferation, Atherosclerosis, Cell Cycle Checkpoints
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
