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In an animal model of acute skin inflammation, loss of PHD1 significantly reduced the overall inflammatory response while increasing cell death within the skin [49]

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Collectively, the in silico findings suggest that SA exerts its biological effects through a multi-target mechanism involving key regulators of oxidative stress, inflammation, and cellular homeostasis

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JAM4, a junctional cell adhesion molecule interacting with a tight junction protein, MAGI-1

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