New research published ahead of print in the journal Function suggests that blocking the expression of the NOX1 enzyme in mice may normalize blood pressure increases associated with elastin insufficiency.
Elastin, a key protein that allows skin and other bodily tissues to return to its usual shape after being stretched, plays an important role in vascular health. People with elastin deficiency diseases, including Williams-Beuren syndrome, have genetic abnormalities in the NCF1 gene that can lead to high blood pressure and stiffening of the arteries, which in turn, may progress to cardiovascular disease.
Researchers found that mice with NOX1 insufficiency, an enzyme encode by the NCF1 gene, had less oxidative stress (cellular damage caused by molecule called reactive oxygen species) and lower blood pressure than those with normal levels of NOX1.
“By lowering the Nox1-mediated capacity for vascular [reactive oxygen species] production, blood pressure differences can be normalized,” the researchers wrote.
Read the full article, “Inhibition of NOX1 mitigates blood pressure increases in elastin insufficiency.” Contact the APS Communications Office to schedule an interview with the research team.
