Recent findings indicate that the senescence-associated secretory phenotype (SASP) is linked to age-related diseases such as cardiovascular conditions, dementia, and metabolic disorders.
is characterized by permanent cell cycle cessation and the release of pro-inflammatory substances.
Accumulation of senescent cells may contribute to aging-related illnesses and functional decline.
Therapeutic strategies like and have shown potential in preclinical and clinical studies.
The effectiveness of these therapies can be influenced by dosing intervals, affecting both their benefits and risks.
Natural lifestyle interventions, including calorie restriction and exercise, may help regulate senescence pathways.
Simplified
BACKGROUND: is a fundamental characteristic of aging, marked by permanent cell cycle cessation and the release of pro-inflammatory mediators. Although senescence plays advantageous roles in tissue regeneration and tumor suppression, its accumulation leads to aging-related illnesses and functional deterioration.
OBJECTIVE: This review examines the processes of cellular senescence, its effects on aging and age-related disorders, and emerging therapeutic strategies to modulate senescence for promoting healthy aging.
METHODS: A thorough literature review was performed using peer-reviewed studies on cellular senescence, its molecular pathways, and therapeutic interventions. Emphasis was placed on , , and lifestyle interventions that modulate senescence-associated pathways. Studies published in Scopus, Web of Science and PubMed between 2014-2025 were selected.
RESULTS: Recent discoveries underscore the dual function of cellular senescence in aging and pathology. The senescence-associated secretory phenotype (SASP) fosters chronic inflammation and tissue dysfunction, connecting senescence to age-related diseases including cardiovascular conditions, dementia, and metabolic disorders. Therapeutic strategies, including senolytics (drugs that specifically eradicate senescent cells) and senomorphics (compounds that suppress SASP without killing cells), show promise in preclinical and clinical studies. Notably, dosing interals (intermittent vs continuous) influence both therapeutic efficacy and adverse events such as thrombocytopenia. Additionally, the state and limitations of clinical validation of aging biomarkers (eg, p16^INK4a, β-galactosidase) remain major hurdles for translation. Lifestyle interventions such as calorie restriction and exercise have also been identified as natural modulators of senescence pathways.
CONCLUSION: Targeting cellular senescence offers a promising avenue for promoting healthy aging and mitigating age-linked diseases. Continued research into senescence-modulating interventions may lead to novel therapeutics designed to prolong healthspan and lifespan.
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