Researchers who identified “notably reduced” Humanin protein levels in patients with age-related macular degeneration (AMD),1 claim their finding corroborates the pivotal role Humanin plays in maintaining tissue homeostasis and normal functioning in the eye. The novel finding could contribute to the development of therapeutics tools for reducing inflammation to alleviate AMD disease pathology.
Armed with the knowledge that inflammatory processes drive the progression of AMD, researchers from the University of California Irvine and University of Southern California compared the protein levels of inflammation markers in normal and AMD retinal pigment epithelial (RPE) transmitochondrial cybrid cells. They investigated the effects of treatment with exogenous Humanin G (HNG), a mitochondrial derived peptide that is cytoprotective in AMD and can protect against mitochondrial and cellular stress induced by damaged AMD mitochondria.
The researchers found differential levels of inflammation proteins between normal and AMD plasma samples. Compared to control plasma samples, AMD plasma showed higher protein levels of inflammation markers. However, plasma levels of endogenous Humanin protein were 36.58% lower in AMD patients compared to those in age-matched normal subjects. After treatment with HNG, the researchers observed a marked reduction in protein levels of inflammation markers that were elevated in AMD RPE transmitochondrial cybrid cells.
“In conclusion, we present novel findings that: a) show reduced Humanin protein levels in AMD plasma vs. normal plasma; b) suggest the role of inflammatory markers in AMD pathogenesis, and c) highlight the positive effects of Humanin G in reducing inflammation in AMD.”