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Revista de Osteoporosis y Metabolismo Mineral

versión On-line ISSN 2173-2345versión impresa ISSN 1889-836X

Resumen

PENA-LARREA, Lorena; DE BLAS-RODRIGUEZ, Manuela; NAVES-DIAZ, Manuel  y  GOMEZ-ALONSO, Carlos. Cellular senescence as a pathogenic factor and potential therapeutic target in osteoporosis. Rev Osteoporos Metab Miner [online]. 2023, vol.15, n.3, pp.115-124.  Epub 08-Mar-2024. ISSN 2173-2345.  https://dx.doi.org/10.20960/revosteoporosmetabminer.00013.

Cellular senescence is a process induced by various types of stress that irreversibly cause cell cycle arrest and changes to the characteristics and functionality of cells, as well as the acquisition of a secretory phenotype that generates a pro-inflammatory environment. While, in certain contexts, it is beneficial for tissues and promotes organism development, senescence is a cellular fate implicated in the process of aging and age-related degenerative conditions. Senolytics are drugs that specifically eliminate senescent cells, and senomorphics are drugs that suppress their senescence-associated secretory phenotype (SASP) without inducing cell death. Therefore, therapeutic strategies targeting senescent cells (senolytics and senomorphics) as an underlying mechanism of aging emerge as an alternative with great potential to fight age-related diseases as a whole rather than individually. One of these conditions is osteoporosis where it has been experimentally described that drugs such as zoledronic acid have effects on preosteoblasts and act on senescent cells extending survival and opening up the possibility of treating age-related diseases with drugs already used in practice, which may have effects beyond the bone itself and increase overall survival. In this study, a review will be conducted in this rapidly growing field in recent years of undeniable translational interest.

Palabras clave : Senescence; Osteoporosis; Senolytics; Senomorphics; Bone; Frailty; Senescence-associated secretory phenotype (SASP).

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