Glycyl-l-histidyl-l-lysine-Cu2+ rescues cigarette smoking-induced skeletal muscle dysfunction via a sirtuin 1-dependent pathway.
Deng M, Zhang Q, Yan L et al. · Journal of cachexia, sarcopenia and muscle · PMID 36905132
Study summary
Main finding
Patients had lower endogenous GHK levels; GHK-Cu improved selected muscle and oxidative-stress measures in cells and mice through SIRT1-related signaling.
Human COPD observations, cultured myotubes, and smoke-exposed mice
How the study was set up
GHK levels in nine people with COPD and 11 healthy controls were compared, alongside smoke-exposure experiments using muscle cells and mice.
What the researchers measured
Blood peptide associations, muscle mass and grip strength, oxidative-stress markers, and SIRT1-related signaling were assessed.
How to read this evidence
This paper combines observations in people with laboratory or animal experiments. Measuring a naturally occurring peptide in people is different from testing peptide administration.
Results in context
The human component was observational; GHK-Cu administration was tested in cells and mice. The study does not establish treatment of COPD-related muscle dysfunction in people.
What this does not establish
The small human sample was observational and measured GHK, not response to GHK-Cu treatment. Experimental benefits cannot establish clinical efficacy.
Publication & source
Why this paper is included
Muscle-cell and smoking-exposed mouse experiments administered GHK-Cu; the accompanying human data measured free GHK.
Publication indexing
Journal Article · Research Support, Non-U.S. Gov't