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For instance, copper is required for the activation of MEK1 kinase, and disruption of this copper-dependent signaling contributes directly to myofibrillar disorganization and pathological hypertrophy [182, 183]

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Rather than acting on a single target, BPC-157 is studied as a pleiotropic agent one that appears to influence several repair pathways at once, with the nitric-oxide (NO) system and angiogenic, growth-factor signalling recurring throughout the literature

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