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This participation contributes to the amplification and persistence of low-grade chronic inflammation within the joint cavity (Hu et al., 2024)
The modification of these macromolecules has deleterious effects on their physiological functions
and GIP receptors have also been demonstrated to activate phosphoinositide 3-kinase (PI3K) and its downstream effector Akt, which modulates mitochondrial function, metabolism, and cell survival
This highlights the intricate relationship between lipid metabolism, cellular signaling and the maintenance of CSC properties
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