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Strategies for targeting senescent cells in human disease
Open accessAbstract
Cellular senescence represents a distinct cell fate characterized by replicative arrest in response to a host of extrinsic and intrinsic stresses. Senescence provides programming during development and wound healing, while limiting tumorigenesis. However, pathologic accumulation of senescent cells is implicated in a range of diseases and age-associated morbidities across organ systems. Senescent cells produce distinct paracrine and endocrine signals, causing local tissue dysfunction and exerting deleterious systemic effects. Senescent cell removal by apoptosis-inducing "senolytic" agents or therapies that inhibit the senescence-associated secretory phenotype, SASP inhibitors, have demonstrated benefit in both pre-clinical and clinical models of geriatric decline and chronic diseases, suggesting senescent cells represent a pharmacologic target for alleviating effects of fundamental aging processes. However, senescent cell populations are heterogeneous in form, function, tissue distribution, and even differ among species, possibly explaining issues of bench-to-bedside translation in current clinical trials. Here, we review features of senescent cells and strategies for targeting them, including immunologic approaches, as well as key intracellular signaling pathways. Additionally, we survey current senolytic therapies in human trials. Collectively, there is demand for research to develop targeted senotherapeutics that address the needs of the aging and chronically-ill.
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“Through upregulation of pro-survival and antiapoptotic pathways such as SRC kinases, the PI3K-AKT signaling pathway, heat shock protein (HSP) pathways, serpines, mitochondrial pathways or apoptosis regulator BCL-2-related proteins, those senescent cells with a proapoptotic SASP can survive, despite the cytotoxic microenvironment they create6,7,14,34,35,54–58.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [58]
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“but also enhance SASP autocrine loop, as found in multiple previous studies,124,125,126,127”
From Single-cell senescence identification reveals senescence heterogeneity, trajectory, and modulators (2024) · cites this paper as [127]
Experimental — accuracy not yet measuredIn the citing paper
“Persistent senescent cells are known to exert detrimental long-term effects on organ function and can promote tumorigenesis33,96,112,177,178.”
From COVID-19 and cellular senescence (2023) · cites this paper as [96]
In the citing paper
“Senescent cells are highly associated with aging and pathological conditions and could be targeted to slow the aging process.”
From The heterogeneity of cellular senescence: insights at the single-cell level (2023) · cites this paper as [3]
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“At the transcript level, p16 and p21 are the two most commonly used markers for senescent cells [3,16].”
From The heterogeneity of cellular senescence: insights at the single-cell level (2023) · cites this paper as [3]
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BackgroundNutrition Interventions of Herbal Compounds on Cellular Senescence
Chen, Z., Wu, Y., Lin, Q., Cai, J., Liu, X., & Liang, Y. (2022) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2022/1059257 · Cited by 8
“Studies have shown that senescent fibroblasts are selectively killed by dasatinib and quercetin (a senolytic) [98].”
The pathological potential of ependymal cells in mild traumatic brain injury
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“Since the accumulation and retention of DNA damage in ependymal cells likely increases their susceptibility to becoming senescent, one therapeutic approach could be the use of senomorphic or senolytic compounds, acting to reduce SASP signaling or eliminate the senescent cells that secrete SASP factors, respectively (G…”
BackgroundExploring senescence as a modifier of β cell extracellular vesicles in type 1 diabetes
Motlagh, R. A., Pipella, J., & Thompson, P. J. (2024) · Frontiers in Endocrinology · doi:10.3389/fendo.2024.1422279 · Cited by 8
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Xu, Q., Li, G., Zhang, H., Jiang, Z., Gao, X., Li, Z., Prata, L. G. P. L., Kirkland, J. L., Zhang, G., & Sun, Y. (2026) · Nature Communications · doi:10.1038/s41467-026-70302-9 · Cited by 6
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“Meanwhile, the levels of ROS clearing enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), are decreased [73], which further facilitating ROS accumulation to cause oxidative damage to macromolecules such as DNA, lipid, and protein, thereby exacerbating…”
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“The accumulation of senescenT-cells in organs and tissues can be partially explained by the reduced efficiency of senescent cell clearance by immune system (Ovadya et al., 2018; Gasek et al., 2021).”
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“This cell-nonau-tonomous transmission is the main pathway through which senescence affects tissue function and organismal health (Gasek et al. 2021).”
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“Recent research continues to explore how these hallmarks contribute to our understanding of the aging process and age-related diseases (Gasek et al. 2021).”
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“11,12 DNA damage contributes to premature cellular senescence by continuously activating the DNA damage response, which induces cellular senescence through the p53 pathway.”
Anti-BCL2 therapy eliminates giant congenital melanocytic nevus by senolytic and immune induction
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“25,26 Senescent cells are characterized by their resistance to apoptosis, which allows them to persist in tissues for extended periods.”
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“These therapeutic strategies are broadly classified into two categories: senolytics and senomorphics (68, 69).”
Langevin dynamics for subdiffusion with senescence effects
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Effect of Ramadan Intermittent Fasting on Autophagy and Gene Expression
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PRDM16 Reduces Cellular Senescence by Upregulating GSTM1
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“However, senescent cells exhibit highly diverse molecular and functional phenotypes and activate antiapoptotic pathways, whereas immunosenes-cence partially weakens the immune system ’ s ability to clear senescent cells (Gasek et al., 2021).”
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“The therapeutic effects observed therefore likely reflect a comprehensive approach: primary intervention through targeted delivery to VCAM1 + pre-senescent endothelial cells, complemented by secondary effects on other senescent cell types within the cardiac microenvironment [28].”
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“In drug design, key proteins within a specific signaling pathway are often targeted as they play a crucial role in causing physiological or biochemical effects in cells (Gasek et al., 2021).”
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“In addition, aging represents a primary risk factor for many degenerative pathologies, such as neurodegenerative diseases, metabolic diseases/diabetes, cardiovascular diseases, and cancer [2].”
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Identification of novel senolytic compounds from natural food sourcesPreprint
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“The signaling pathway is responsible for inhibiting apoptosis related mechanisms that would otherwise cause the senescent cell to undergo apoptosis (Gasek et al., 2021).”
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Metadata
- Authors
- Gasek, N. S., Kuchel, G. A., Kirkland, J. L., & Xu, M.
- Affiliations
- University of Connecticut (US)
- Mayo Clinic (US)
- Corresponding author
- Xu, Ming
- Venue
- Nature Aging
- Published
- 2021-10-07
- Volume
- 1
- Issue
- 10
- Pages
- 870-879
- ISSN
- 2662-8465 (ISSN-L)
- PMC
- PMC8612694
- OpenAlex
- W3202997660
- Cited by
- 501
- References
- 152
- Citations by year
- 2026: 78 · 2025: 120 · 2024: 141 · 2023: 95 · 2022: 63 · 2021: 4
- FWCI
- 10.10
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Nature Aging (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Health & Human Services | NIH | National Institute on Aging (R21AG063528,R33AG061456, R37AG013925, R01AG072301, P01AG062413, R21AG063528,R03AG072374,R01AG066679, R01AG068860)
- 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, senolytics, senescence-associated secretory phenotype, senolytic therapy, senotherapeutics, aging, age-related diseases, intracellular signaling, bench-to-bedside translation, chronic disease
- MeSH terms
- Senescence-Associated Secretory Phenotype, Aging, Cell Differentiation, Chronic Disease, Humans, Signal Transduction, Cellular Senescence
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