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PPARα activator fenofibrate inhibits myocardial inflammation and fibrosis in angiotensin II-infused rats
Abstract
Background Peroxisome proliferator-activated receptor (PPAR)alpha is highly expressed in the heart. PPAR alpha may play a role in cardiac hypertrophy, but effects on cardiac function, inflammation, and fibrosis are unknown. We tested the hypothesis that the PPAR alpha activator fenofibrate prevents myocardial inflammation and fibrosis in angiotensin (Ang) II-infused rats. Methods and results Sprague Dawley rats received Ang II (120 ng/kg/min subcutaneously), fenofibrate (100 mg/kg/d p.o.), or Ang II + fenofibrate. After 7 d, systolic blood pressure (mmHg) was elevated (P < 0.01) in Ang II-infused rats (173 +/- 4) vs. controls (115 +/- 2) and reduced by fenofibrate (137 +/- 5). Electrophoretic mobility shift assay demonstrated that Ang II upregulated cardiac nuclear factor kappa B activity by 50%. Ang II significantly increased cardiac expression of vascular-cell adhesion molecule-1, platelet endothelial cell adhesion molecule, and intercellular adhesion molecule-1. Increases in expression of these inflammatory mediators were normalized by fenofibrate. Ang II-induced expression of transforming growth factor-beta 1, collagen deposition, and macrophage infiltration were partially prevented by fenofibrate. Conclusions The PPAR alpha activator fenofibrate prevented development of hypertension, and improved myocardial inflammation and collagen deposition in Ang II-infused rats. The hypolipidemic drug fenofibrate may be useful in prevention and treatment of myocardial disease associated with hypertension and hyperlipidemia.
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“Diep et al. [101] and Goya et al. [102] reported that FF increases endothelial Nitric Oxide (NO) availability.”
From Fenofibrate and metabolic syndrome (2010) · cites this paper as [101]
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Metadata
- Authors
- Diep, Q.
- Affiliations
- Montreal Clinical Research Institute (CA)
- Corresponding author
- Diep, Q
- Venue
- Journal of Molecular and Cellular Cardiology
- Publisher
- Elsevier BV
- Published
- 2004-02
- Volume
- 36
- Issue
- 2
- Pages
- 295-304
- ISSN
- 0022-2828 (ISSN-L)
- OpenAlex
- W2081813895
- Cited by
- 165
- References
- 34
- Citations by year
- 2026: 2 · 2024: 3 · 2023: 3 · 2022: 2 · 2021: 4 · 2020: 4 · 2019: 1 · 2018: 5 · 2017: 3 · 2016: 6 · 2015: 7 · 2014: 6 · 2013: 7 · 2012: 7
- FWCI
- 7.59
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Molecular and Cellular Cardiology (publishedVersion)
- PubMed (publishedVersion)
- University of Regensburg Publication Server (University of Regensburg) (acceptedVersion)
- Funders
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Keywords
- fenofibrate, PPARα, angiotensin II, myocarditis, myocardial fibrosis, hypertension, NF-κB, adhesion molecules, TGF-β1, collagen deposition, macrophage infiltration, hyperlipidemia, cardioprotection
- MeSH terms
- Angiotensin II, Animals, Blood Pressure, Collagen, Electrocardiography, Fibrosis, Heart, Hypertension, Inflammation, Infusions, Intravenous, Myocardium, Fenofibrate, Transcription Factors, Transforming Growth Factor beta, NF-kappa B, Rats, Sprague-Dawley, Receptors, Cytoplasmic and Nuclear, Intercellular Adhesion Molecule-1, Rats, Transforming Growth Factor beta1
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