Impaired endothelial nitric oxide synthase (eNOS) function and decreased nitric oxide (NO) production are linked to cardiovascular disease risk factors like diabetes and obesity, affecting mitochondrial health.
Genetic eNOS deletion and short-term NOS inhibition in rodents led to reduced mitochondrial protein levels and disrupted fission/fusion processes in the aorta.
The study highlights the importance of eNOS/NO in maintaining both baseline and adaptive mitochondrial biogenesis within blood vessels, which is crucial for cardiovascular health.