Mitochondrial CypD Acetylation Promotes Endothelial Dysfunction and Hypertension.

ABSTRACT:

Background

Nearly half of adults have hypertension, a major risk factor for cardiovascular disease. Mitochondrial hyperacetylation is linked to hypertension, but the role of acetylation of specific proteins is not clear. We hypothesized that acetylation of mitochondrial CypD (cyclophilin D) at K166 contributes to endothelial dysfunction and hypertension.

Methods

To test this hypothesis, we studied CypD acetylation in patients with essential hypertension, defined a pathogenic role of CypD acetylation in deacetylation mimetic CypD-K166R mutant mice and endothelial-specific GCN5L1 (general control of amino acid synthesis 5 like 1)-deficient mice using an Ang II (angiotensin II) model of hypertension.

Results

Arterioles from hypertensive patients had 280% higher CypD acet

SUBMITTER: Dikalova A 

PROVIDER: S-EPMC11116043 | biostudies-literature | 2024 May

REPOSITORIES: biostudies-literature