Researchers used gene therapy to overexpress VEGFB186 in 18-month-old mice, successfully reversing key aspects of cardiac aging. The treatment prevented age-related diastolic dysfunction, reduced heart fibrosis, and restored nerve fiber density. While VEGFB induced some cardiac hypertrophy, this appeared compensatory rather than harmful. The therapy worked by activating the STAT3 pathway and improving heart rate variability. These findings suggest VEGFB could become a promising therapeutic target for combating age-related heart decline in humans.
