Number of the records: 1  

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

  1. 1.
    SYSNO ASEP0456654
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleNitrated 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 authors16
    Source TitleCardiovascular Research - ISSN 0008-6363
    Roč. 109, č. 1 (2016), s. 174-184
    Number of pages11 s.
    Publication formPrint - P
    Languageeng - English
    CountryNL - Netherlands
    KeywordsAtrial fibrillation ; Fibrosis ; Nitro-fatty acids
    Subject RIVBO - Biophysics
    R&D ProjectsGP13-40824P GA ČR - Czech Science Foundation (CSF)
    EE2.3.30.0030 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    Institutional supportBFU-R - RVO:68081707
    UT WOS000368414600018
    DOI10.1093/cvr/cvv254
    AnnotationAim 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.
    WorkplaceInstitute of Biophysics
    ContactJana Poláková, polakova@ibp.cz, Tel.: 541 517 244
    Year of Publishing2016
Number of the records: 1  

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