PMID-36905132 – GHK-Cu Rescues Smoking-Induced Skeletal Muscle Dysfunction via SIRT1
Deng M et al. "Glycyl-L-histidyl-L-lysine-Cu2+ rescues cigarette smoking-induced skeletal muscle dysfunction via a sirtuin 1-dependent pathway," Journal of Cachexia, Sarcopenia and Muscle, 2023;14(3):1365-1377. doi:10.1002/jcsm.13213
Quick Reference
| Property | Value |
|---|---|
| PMID | 36905132 |
| DOI | 10.1002/jcsm.13213 |
| Year | 2023 |
| Journal | Journal of Cachexia, Sarcopenia and Muscle |
| Study Type | Animal in vivo + in vitro (with human biomarker data) |
| Evidence Level | III |
| Sample | COPD patients (plasma GHK levels) + mouse CS exposure model + C2C12 cells |
| Peptide(s) Studied | GHK-Cu |
Key Findings
- Plasma GHK levels significantly decreased in COPD patients vs. healthy controls (human data)
- GHK-Cu protected against cigarette smoke-induced skeletal muscle dysfunction in mice
- Mechanism: SIRT1 (sirtuin 1) activation pathway
- Improved grip strength and reduced muscle loss in treated mice
- Published in high-impact journal (IF ~9.4)
Study Design
Multi-component study: (1) Human plasma measurement of GHK levels in COPD vs. control patients; (2) Mouse model of cigarette smoke-induced muscle dysfunction with GHK-Cu treatment; (3) In vitro C2C12 myotube experiments for mechanistic pathway analysis (SIRT1).
Limitations
- Human component limited to biomarker measurement (plasma GHK levels); no human therapeutic intervention
- Mouse model may not reflect chronic COPD muscle wasting in humans
- SIRT1 pathway activation needs validation in human muscle tissue
Clinical Relevance
Highest-impact publication in the GHK-Cu literature (Journal of Cachexia, Sarcopenia and Muscle). Notably includes human data (decreased plasma GHK in COPD). The SIRT1 pathway connection links GHK-Cu to the sirtuin/longevity biology. Evidence Level III due to inclusion of human biomarker data. Relevant for sarcopenia and anti-aging applications.
Related
#research #animal-in-vivo #evidence-level-III