“Youth” Protein Might Be Key for Prevention of Age-related Eye Diseases

A new mouse-model study, conducted by the National Eye Institute, finds that the loss of a certain protein could cause retinal pigment epithelium (RPE) cells to stop nourishing and recycling photoreceptor cells. The research team also finds that the “youth” protein, pigment epithelium-derived factor (PEDF), protects cells in the eye’s retina from oxidative stress.Youth Protein Might Be Key for Prevention of Age-related Eye Diseases

For this study, the research team used a mouse model bioengineered without the PEDF gene Serpinf1. The RPE cell nuclei were enlarged, which could indicate differences in how the cells’ DNA was arranged. These cells had also activated 4 genes linked to cellular senescence and aging.

Senior investigator Dr. Patricia Becerra explains: “Telomeres are a structure at the end of a chromosome that maintains the integrity of our genes and are a critical factor for age-related diseases. Their shortening can affect the expression of genes during aging; the PEDF gene, Serpinf1, is one of them,” she continued.

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