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Targeting Senescence: A Review of Senolytics and Senomorphics in Anti-Aging Interventions

Saliev, Timur, Singh, Prim B.·2025·Biomolecules
DOI 10.3390/biom15060860PMC PMC12190739
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Abstract

Cellular senescence is a fundamental mechanism in aging, marked by irreversible growth arrest and diverse functional changes, including, but not limited to, the development of a senescence-associated secretory phenotype (SASP). While transient senescence contributes to beneficial processes such as tissue repair and tumor suppression, the persistent accumulation of senescent cells is implicated in tissue dysfunction, chronic inflammation, and age-related diseases. Notably, the SASP can exert both pro-inflammatory and immunosuppressive effects, depending on cell type, tissue context, and temporal dynamics, particularly in early stages where it may be profibrotic and immunomodulatory. Recent advances in senotherapeutics have led to two principal strategies for targeting senescent cells: senolytics, which selectively induce their apoptosis, and senomorphics, which modulate deleterious aspects of the senescence phenotype, including the SASP, without removing the cells. This review critically examines the molecular mechanisms, therapeutic agents, and clinical potential of both approaches in the context of anti-aging interventions. We discuss major classes of senolytics, such as tyrosine kinase inhibitors, BCL-2 family inhibitors, and natural polyphenols, alongside senomorphics including mTOR and JAK inhibitors, rapalogs, and epigenetic modulators. Additionally, we explore the biological heterogeneity of senescent cells, challenges in developing specific biomarkers, and the dualistic role of senescence in physiological versus pathological states. The review also highlights emerging tools, such as targeted delivery systems, multi-omics integration, and AI-assisted drug discovery, which are advancing precision geroscience and shaping future anti-aging strategies.

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  • Senescent cells can evade elimination by upregulating alternative survival pathways such as MCL-1 or modulating immune checkpoints.

    “the capacity of SnCs to evade elimination by upregulating alternative survival pathways (such as MCL-1)54,55 or modulating immune checkpoints underscore the need for more sophisticated therapeutic approaches56.”

    From Emerging strategies in senotherapeutics: from broad-spectrum senolysis to precision reprogramming (2026) · cites this paper as [56]

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Metadata

Authors
Saliev, T., & Singh, P. B.
Venue
Biomolecules
Publisher
MDPI AG
Published
2025-06-13
Volume
15
Issue
6
Pages
860
ISSN
2218-273X
DOI
10.3390/biom15060860
PMC
PMC12190739
Cited by
160
References
4
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
Ministry of Science and Higher Education of the Republic of Kazakhstan (BR24992900)

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