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Rather than indiscriminately blocking macrophage activity (which would impair the early inflammatory debridement phase of wound healing), GHK-Cu research documents a shift in macrophage phenotype from pro-inflammatory M1 toward the anti-inflammatory, pro-healing M2 profile at later stages of the inflammatory response
This mechanistic insight positions CPT as a targeted modulator of mitochondrial RET, linking structural complex I regulation to redox homeostasis and neuronal survival, and underscores its therapeutic potential in PD
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1993 Oct;8(10):1657-62
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