17-Β-Estradiol Protects Chondrocytes From Senescence And Ameliorates Osteoarthritis Progression Via Erα-AKT-Foxo4 Pathway
Osteoarthritis, a common and debilitating joint disease, often involves the breakdown of cartilage, the flexible tissue that cushions our joints. This breakdown is partly due to cartilage cells, called chondrocytes, undergoing a process called senescence, where they stop dividing and can even release harmful substances. Recent research sheds light on how a natural hormone, 17-β-estradiol (a type of estrogen), might offer protection against this process. Studies indicate that 17-β-estradiol helps keep chondrocytes healthy and prevents them from aging prematurely. This protective effect is crucial because it can slow down the overall progression of osteoarthritis. The mechanism behind this involves a complex cellular communication network. 17-β-estradiol interacts with a specific receptor within cells, known as Estrogen Receptor alpha (ERα). This interaction then triggers a cascade of events, activating a key signaling pathway called AKT. The activated AKT pathway, in turn, influences another protein, FOXO4, which plays a role in cell survival and stress response. By modulating this ERα-AKT-FOXO4 pathway, 17-β-estradiol helps maintain the health and function of chondrocytes, ultimately contributing to the amelioration of osteoarthritis.
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