Mechanisms and therapeutic implications of cellular senescence in osteoarthritis

The development of osteoarthritis (OA) correlates with a rise in the number of senescent cells in joint tissues, and the senescence-associated secretory phenotype (SASP) has been implicated in cartilage degradation and OA. Age-related mitochondrial dysfunction and associated oxidative stress might induce senescence in joint tissue cells. However, senescence is not the only driver of OA, and the mechanisms by which senescent cells contribute to disease progression are not fully understood. Furthermore, it remains uncertain which joint cells and SASP-factors contribute to the OA phenotype. Research in the field has looked at developing therapeutics (namely senolytics and senomorphics) that eliminate or alter senescent cells to stop disease progression and pathogenesis. A better understanding of how senescence contributes to joint dysfunction may enhance the effectiveness of these approaches and provide relief for patients with OA. The development of osteoarthritis (OA) correlates with an increase in the number of senescent cells in joint tissues and the senescence-associated secretory phenotype is implicated in cartilage degradation and OA. Eliminating or altering senescent cells with senolytics or senomorphics could stop OA progression and pathogenesis.

Automated summary

The development of osteoarthritis (OA) is correlated with an increase in senescent cells in joint tissues, with senescence-associated secretory phenotype (SASP) implicated in cartilage degradation and OA. Developing therapeutics like senolytics or senomorphics to eliminate or alter senescent cells may halt the progression and pathogenesis of OA.