Nitrated fatty acids suppress angiotensin II-mediated fibrotic remodelling and atrial fibrillation.

ABSTRACT:

Aim

Atrial fibrosis, one of the most striking features in the pathology of atrial fibrillation (AF), is promoted by local and systemic inflammation. Electrophilic fatty acid nitroalkenes, endogenously generated by both metabolic and inflammatory reactions, are anti-inflammatory mediators that in synthetic form may be useful as drug candidates. Herein we investigate whether an exemplary nitro-fatty acid can limit atrial fibrosis and AF.

Methods and results

Wild-type C57BL6/J mice were treated for 2 weeks with angiotensin II (AngII) and vehicle or nitro-oleic acid (10-nitro-octadec-9-enoic acid, OA-NO2, 6 mg/kg body weight) via subcutaneous osmotic minipumps. OA-NO2 significantly inhibited atrial fibrosis and depressed vulnerability for AF during right atrial electrophysiologi

SUBMITTER: Rudolph TK 

PROVIDER: S-EPMC5901131 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature