A new University of Maryland-led discovery could spur the development of new and improved treatments for Hutchinson-Gilford progeria syndrome (HGPS), a rare genetic disorder with no known cure that causes accelerated aging in children. Published in the journal Aging Cell on October 18, 2024, in collaboration with researchers from the National Institutes of Health (NIH) and Duke University, the study identified a protein linked to the cardiovascular health of animal models with progeria that could translate to human treatments. Heart failure and stroke are the most common causes of death for people with HGPS, who typically have a life expectancy between 6 and 20 years old.
These new findings from the lab of UMD Cell Biology and Molecular Genetics Professor Kan Cao are "highly promising," according to lead author and biological sciences Ph.D. student Sahar Vakili.
"This could pave the way for new treatments targeting cardiovascular complications in HGPS, which are currently a major cause of mortality in the affected children," Vakili said. Beyond progeria, insights gained from this research might also be applicable to other age-related diseases where endothelial dysfunction plays a role." Sahar Vakili, University of Maryland Sometimes called the "Benjamin Button disease," HGPS causes a variety of symptoms associated with aging, including skin wrinkling, joint stiffness, and the loss of hair and body fat.
The disease stems from a mutation in the LMNA (lamin A) gene, which produc.