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However, it is also unknown if the PI3K/AKT pathway promotes KFb cell function by regulating glucose metabolism under hypoxic conditions. The amount of mitochondrial membrane potential increased after the PI3K/AKT pathway was activated with LY294002 inactivation, according to here, while mitochondrial membrane potential increased when LY294002 was activated. In addition, cell proliferation was impaired when KFb were treated with both SC79 and 2U2010deoxyu2010glucose, compared to the SC79 group. The PI3K/AKT pathway in KFb under hypoxia helps proliferation and inhibits apoptosis by limiting glycolysis, according to our findings, indicating that the PI3K/AKT signaling pathway could be a therapeutic target for keloids.
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