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The mechanisms driving central sensitization include elevated substance P, reduced descending pain inhibition, altered glutamate signaling, and microglial activation in the central nervous system

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It shares wound healing overlap with GHK-Cu but through entirely different molecular mechanisms

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Furthermore, another study focusing on GC revealed that MACC1 enhances MET expression and stimulates the downstream AKT/mTOR pathway, which consequently leads to increased PD-L1 expression levels in GC [132]