NIH R01 · 2024
Sirtuin 3 Inactivation and SOD2 Acetylation in Vascular Dysfunction and Hypertension
Project Summary Vascular dysfunction plays a key role in hypertension and cardiovascular disease associated with inactivation of mitochondrial deacetylase Sirt3, but mitochondria-targeted treatments are not available. Sirt3 inactivation induces inhibition of mitochondrial superoxide dismutase (SOD2) and impairs fatty acid metabolism leading to mitochondrial oxidative stress and formation of harmful lipid peroxidation products, isolevuglandins (isoLG). We suggest that a feed- forward cycle between Sirt3 inactivation and mitochondrial isoLG promotes vascular dysfunction and hypertension. We developed new mitochondria-targeted isoLG scavenger, mito2HOBA, which protects Sirt3 activity and…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.