Study summary · research use only
17-β-Estradiol Protects Chondrocytes From Senescence and Ameliorates Osteoarthritis Progression via ERα-AKT-FOXO4 Pathway
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this study (osteoarthritic chondrocytes; rat model of surgery-induced osteoarthritis in vivo), the authors examined 17-β-Estradiol (E2) and chondrocyte senescence. E2 was reported to counter multiple types of chondrocyte senescence via oestrogen receptor α (ERα), activating AKT and promoting nuclear export and degradation of FOXO4. Knockdown of FOXO4 in osteoarthritic chondrocytes was associated with reduced cellular senescence. Intra-articular E2 injection was associated with amelioration of surgery-induced osteoarthritis in the rat model. The authors describe E2 as acting through the ERα-AKT-FOXO4 pathway to influence chondrocyte senescence and osteoarthritis progression in this model.
Abstract
Osteoarthritis (OA) is a prevalent cause of joint pain in elderly individuals, and chondrocyte senescence plays a crucial role in its pathogenesis. FOXO4 has been identified as a crucial molecule in cellular senescence. However, little is known regarding its role in OA and the regulation of its expression. 17-β-Estradiol (E2) has been demonstrated to exert a protective effect in OA, yet the underlying mechanism remains largely unexplained. In this study, we reported a protective effect of E2 against multiple types of chondrocyte senescence, and this effect was mediated by oestrogen receptor α (ERα). Mechanically, E2 activated AKT and facilitated the nuclear export and the degradation of FOXO4, which played a crucial role in resisting senescence. Moreover, knockdown of FOXO4 in osteoarthritic chondrocytes alleviated cellular senescence. Furthermore, we demonstrated that intra-articular injection of E2 was effective in ameliorating surgery-induced OA in a rat model. Collectively, E2 contributed to the alleviation of chondrocyte senescence through the ERα-AKT-FOXO4 signalling pathway and ameliorated OA progression in the rat model. Our study offers a novel therapeutic approach for controlling chondrocyte senescence and provides insights into the role of E2 in treating OA.
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