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Additionally, it has been described that estrogens can regulate the differentiation of endothelial progenitor cells derived from bone marrow through mechanisms that include an increase in Akt phosphorylation and modulation of the telomerase activity, which consequently delays the onset of senescence (Imanishi et al., 2005)

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Its persistence sustains inflammation, limits therapeutic access, and accelerates structural joint damage, making targeted modulation of fibrotic pathways a critical priority for improving long-term outcomes in chronic gout