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This pathway involving PPAR upregulation and consequent downregulation of TGF-1, CTGF, and PDGF positions GHRP-2 as a research tool for studying CD36-mediated anti-fibrotic biology alongside GHRP-6, with GHRP-2s higher GHS-R1a potency enabling comparative research models where dual GHS-R1a/CD36 stimulation intensity is a variable

( Epub 20100821 )

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