Apigenin as a bioactive compound for longevity: Targets and mechanisms in senescent cells
DOI:
https://doi.org/10.31989/bchd.v9i3.1929Resumo
Bioactive compounds have emerged as a focal point in contemporary health and biomedical research due to their potential in disease prevention, health promotion, and longevity enhancement. With the global rise of the longevity movement, attention has increasingly shifted toward understanding how functional foods and bioactive compounds influence molecular mechanisms associated with aging. This review focuses on apigenin, a naturally occurring flavonoid found in many fruits, vegetables, and herbs. Although apigenin exhibits poor bioavailability due to limited solubility and rapid metabolism, it has been shown to exert multiple effects due to its longevity and cellular health.
In terms of cellular senescence, apigenin exhibits senomorphic activity, modulating the senescent cell phenotype rather than directly inducing their death. Specifically, it suppresses the senescence-associated secretory phenotype (SASP) by inhibiting key inflammatory signaling pathways such as NF-κB and p38-MAPK, thereby reducing chronic inflammation and tissue degeneration. However, evidence for its senolytic activity remains inconclusive, as current findings have not shown direct senolytic effects in senescent cell models.
Interestingly, studies in other cellular systems show that apigenin can modulate molecular pathways associated with apoptosis, including the regulation of Bcl-2 family proteins and caspase activation, which may indirectly support cellular renewal processes. Given these findings, apigenin stands out as a promising candidate for further development as a functional ingredient in longevity-focused nutrition. Its potential role as a bioactive modulator of senescent cell behavior highlights new opportunities for future research in nutraceuticals and functional food innovation aimed at promoting healthy aging.
Novelty of the study: This review highlights apigenin as a longevity-oriented functional food bioactive that targets senescent cells through senomorphic mechanisms and NAD⁺ modulation via CD38 inhibition, distinguishing it from previously reported conventional senolytic compounds.
Keywords: apigenin, NAD+ metabolism, CD38 inhibitor, cellular senescence, Senescence-associated secretory phenotype (SASP)
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Copyright (c) 2026 Kamon Chaiyasit, Kadesanee Likitkriengkri, Kanokpong Muangsri, Varit Srisukthaveerat
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