review · Cells
Cellular senescence influences aging, tissue maintenance, and disease progression through the senescence-associated secretory phenotype. This secretory activity releases cytokines, chemokines, growth factors, and matrix-remodelling enzymes. While temporary secretion supports wound repair, chronic presence leads to persistent inflammation, fibrosis, and cancer development. Therapeutic approaches primarily focus on two avenues: eliminating senescent cells entirely or modulating their secretions to curb harmful inflammation while retaining tissue repair functions. Key molecular pathways controlling these processes include NF-κB, C/EBPβ, and cGAS-STING. These mechanisms can potentially be targeted using pharmacological agents, immunotherapies, gene-editing techniques, and epigenetic interventions. Because secretory profiles vary significantly across different tissues, targeted clinical interventions will require tissue-specific biomarkers to guide personalised treatments and address key challenges surrounding immune interactions and long-term safety.
Cellular aging influences chronic disease, tissue damage, and cancer through chemical signals released into surrounding tissues. Learning how to selectively halt harmful inflammation while preserving the natural healing capabilities of these cells could lead to more effective treatments for age-related conditions, organ repair, and cancer, supporting the future design of safer, personalised medical therapies.
This research outlines therapeutic concepts relevant to pharmaceutical and biotechnology developers working on aging, oncology, and regenerative medicine. Potential applications span drug discovery, gene editing, and immunotherapy aimed at specific molecular pathways. The research represents early-stage insights, requiring the identification of tissue-specific biomarkers, long-term safety validation, and multi-omics or artificial intelligence integration before clinical and commercial use can be realised.
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Cellular senescence regulates aging, tissue maintenance, and disease progression through the Senescence-Associated Secretory Phenotype (SASP), a secretory profile of cytokines, chemokines, growth factors, and matrix-remodeling enzymes. While transient SASP aids wound healing, its chronic activation drives inflammation, fibrosis, and tumorigenesis. This review examines SASP's molecular regulation, dual roles in health and pathology, and therapeutic potential. The following two main strategies are explored: senescence clearance, which eliminates SASP-producing cells, and SASP modulation, which refines secretion to suppress inflammation while maintaining regenerative effects. Key pathways, including NF-κB, C/EBPβ, and cGAS-STING, are discussed alongside pharmacological, immunotherapeutic, gene-editing, and epigenetic interventions. SASP heterogeneity necessitates tissue-specific biomarkers for personalized therapies. Challenges include immune interactions, long-term safety, and ethical considerations. SASP modulation emerges as a promising strategy for aging, oncology, and tissue repair, with future advancements relying on multi-omics and AI-driven insights to optimize clinical outcomes.
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DOI: 10.3390/cells14080608
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