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Nitrated fatty acids suppress angiotensin II-mediated fibrotic remodelling and atrial fibrillation
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SYSNO ASEP 0456654 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Nitrated fatty acids suppress angiotensin II-mediated fibrotic remodelling and atrial fibrillation Author(s) Rudolph, T.K. (DE)
Ravekes, T. (DE)
Klinke, A. (DE)
Friedrichs, K. (DE)
Mollenhauer, M. (DE)
Pekarová, Michaela (BFU-R) RID
Ambrožová, Gabriela (BFU-R) RID
Martíšková, Hana (BFU-R) ORCID
Kaur, J.J. (DE)
Matthes, B. (DE)
Schwoerer, A. (DE)
Woodcock, S.R. (US)
Kubala, Lukáš (BFU-R) RID, ORCID
Freeman, B.A. (US)
Baldus, S. (DE)
Rudolph, V. (DE)Number of authors 16 Source Title Cardiovascular Research - ISSN 0008-6363
Roč. 109, č. 1 (2016), s. 174-184Number of pages 11 s. Publication form Print - P Language eng - English Country NL - Netherlands Keywords Atrial fibrillation ; Fibrosis ; Nitro-fatty acids Subject RIV BO - Biophysics R&D Projects GP13-40824P GA ČR - Czech Science Foundation (CSF) EE2.3.30.0030 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) Institutional support BFU-R - RVO:68081707 UT WOS 000368414600018 DOI 10.1093/cvr/cvv254 Annotation 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 electrophysiological stimulation to levels observed for AngII-naive animals. Left atrial epicardial mapping studies demonstrated preservation of conduction homogeneity by OA-NO2. The protection from fibrotic remodelling was mediated by suppression of Smad2-dependent myofibroblast transdifferentiation and inhibition of Nox2-dependent atrial superoxide formation. Workplace Institute of Biophysics Contact Jana Poláková, polakova@ibp.cz, Tel.: 541 517 244 Year of Publishing 2016
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