The alpha-1A adrenergic receptor regulates mitochondrial oxidative metabolism in the mouse heart.

ABSTRACT:

Aims

The sympathetic nervous system regulates numerous critical aspects of mitochondrial function in the heart through activation of adrenergic receptors (ARs) on cardiomyocytes. Mounting evidence suggests that α1-ARs, particularly the α1A subtype, are cardioprotective and may mitigate the deleterious effects of chronic β-AR activation by shared ligands. The mechanisms underlying these adaptive effects remain unclear. Here, we tested the hypothesis that α1A-ARs adaptively regulate cardiomyocyte oxidative metabolism in both the uninjured and infarcted heart.

Methods

We used high resolution respirometry, fatty acid oxidation (FAO) enzyme assays, substrate-specific electron transport chain (ETC) enzyme assays, transmission electron microscopy (TEM) and proteomics to characteriz

SUBMITTER: Sandroni PB 

PROVIDER: S-EPMC10861168 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature