Accumulated DNA damage in the retina is a key contributor to AMD
This study was published online in the journal Aging Cell and reveals how DNA damage compromises the retina’s function and accelerates vision loss.
(Image credit: AdobeStock/Cagkan)
Researchers have found that accumulated DNA damage in the retina is a key contributor to age-related macular degeneration (AMD) and that targeting specific retinal cell types may lead to treatments that slow or stop progression. This study was published online in the journal Aging Cell and reveals how DNA damage compromises the retina’s function and accelerates vision loss.1
Dorota Skowronska-Krawczyk, a University of California (UC) Irvine associate professor of physiology and biophysics and co-corresponding author spoke to these findings in the university’s news release1, saying, “Our findings highlight the critical role DNA damage repair plays in maintaining retina health for good vision. Because age is the strongest risk factor for AMD, gaining deeper insights into the underlying biology of aging in the eye is essential for developing effective therapies.”
The retina’s exposure to light and intense metabolic activity makes it highly vulnerable to oxidative stress and the accumulation of DNA damage over time, a process closely linked to aging. Understanding the delicate relationship between the retina and the retinal pigment epithelium and the basic mechanism driving age-related changes is crucial for developing new approaches to combat AMD.1
The team compared a mouse model with reduced levels of ERCC1-XPF, a DNA repair enzyme, with both young, healthy mice and naturally aging mice. By 3 months of age, the model showed signs of visual impairment, structural alterations in the retina, abnormal blood vessel formation, and shifts in gene expression and metabolism, as well as mitochondrial dysfunction in the retinal pigment epithelium. All these changes mirror those seen in natural human eye aging.1
Skowronska-Krawczyk weighed in on the value of this research: “The more we know about how DNA damage contributes to eye diseases like AMD, [the better] we can develop interventions that address the root causes of vision loss. These could include strategies to counteract oxidative stress, enhance DNA repair or even remove damaged cells before they cause harm. We plan to investigate which cell types drive age-related changes by selectively impairing DNA mechanisms. Our goal is to advance the development of preventative interventions that significantly reduce the burden of age-related vision loss and improve the quality of life for millions.”1
In addition to Skowronska-Krawczyk, members of the research team included William Cho, UC Irvine physiology and biophysics project scientist; co-corresponding author Dr. Laura J. Niedernhofer, professor and director of the University of Minnesota Institute on the Biology of Aging & Metabolism; and faculty and students from the University of Minnesota, the University of Florida and Columbia University.1
The university noted that this work was supported by the University of Minnesota Foundation and a generous donation from Cecilee Faster; and National Institutes of Health grants R01 AG063543, U19AG056278, U54AG079754 and P30 EY034070.1
