Research

Aging is an accumulation of events that occurs in one’s life span. The concept of mitochondrial dysfunction has been set forth as a central theme in multiple aging-related disease states, including cancer, diabetes, and neurodegeneration. In particular, the aging process has been noted to involve deterioration in mitochondrial function. Several theories related to the causes of mitochondrial dysfunction have been proposed, including accumulation of mtDNA mutations, cumulative oxidative damage, and the “mitochondrial theory of aging”. Recent studies identified a novel mitochondrial-derived peptide (MDP) named humanin. Humanin (HN) is a 24 amino-acid peptide, encoded from the 16S ribosomal RNA region of the mitochondrial DNA, originally described as a neurosurvival factor capable of antagonizing Alzheimer’s disease-related cell death insults. We have also shown that HN has potent actions on many processes related to aging, such as development in zebrafish, insulin sensitization, and beta-cell function.

Traditionally, the mitochondrial genome has been annotated as having only 13 protein coding genes, 2 rRNAs, 22 tRNAs and no known introns. Humanin (HN) is a recently discovered, 24-amino acid peptide whose open reading frame (ORF) is found within 16S rRNA gene. Like a Russian nesting doll, it is a gene within a gene within the mitochondrial genome of an organelle within a cell. The discoveries of humanin as a novel, stress responsive and cytoprotective peptide has opened a new field of research.