Cited by 165Cardiac Fibrosis and RemodelingPeroxisome Proliferator-Activated ReceptorsRenin-Angiotensin System Studies

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PPARα activator fenofibrate inhibits myocardial inflammation and fibrosis in angiotensin II-infused rats

Diep, Q·2004·Journal of Molecular and Cellular Cardiology

DOI 10.1016/j.yjmcc.2003.11.004

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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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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)
DOI: 10.1016/j.yjmcc.2003.11.004
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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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PPARα activator fenofibrate inhibits myocardial inflammation and fibrosis in angiotensin II-infused rats

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