Mechanistically, GHK-Cu preserved mitochondrial function by increasing mitochondrial membrane potential, alleviating age-related mitochondrial network fragmentation, shifting mitochondrial dynamics toward fusion via regulating drp-1 and fzo-1 expression, and promoting ATP biosynthesis
Chest 150, 11411157
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Funding This work was partially supported by the Puerto Rico Science, Technology and Research Trust award, and the following grants from the National Institutes of Health: NIGMS/MBRS Grant GM08224, NIMHD RCMI-Infectious and Global Diseases Center Grant G12MD007600, and NIMHD CCRHD-Tropical Emerging Infectious Diseases Research Center Grant U54MD007600
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