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  • 1.
    Castiglioni, Laura
    et al.
    Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy..
    Pignieri, Alice
    Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy..
    Fiasche, Melania
    Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy..
    Giudici, Marco
    KTH, School of Engineering Sciences in Chemistry, Biotechnology and Health (CBH), Centres, Wallenberg Center for Protein Research. Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy..
    Crestani, Maurizio
    Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy..
    Mitro, Nico
    Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy..
    Abbate, Mauro
    IRCCS Ist Ric Farmacol Mario Negri, Ctr Anna Maria Astori, Sci & Technol Pk Kilometro Rosso, Bergamo, Italy..
    Zoja, Carlamaria
    IRCCS Ist Ric Farmacol Mario Negri, Ctr Anna Maria Astori, Sci & Technol Pk Kilometro Rosso, Bergamo, Italy..
    Rottoli, Daniela
    IRCCS Ist Ric Farmacol Mario Negri, Ctr Anna Maria Astori, Sci & Technol Pk Kilometro Rosso, Bergamo, Italy..
    Foray, Claudia
    IRCCS Ist Ric Farmacol Mario Negri, Dept Cardiovasc Res, Milan, Italy..
    Fiordaliso, Fabio
    IRCCS Ist Ric Farmacol Mario Negri, Dept Cardiovasc Res, Milan, Italy..
    Guerrini, Uliano
    Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy..
    Tremoli, Elena
    Ctr Cardiol Monzino, Milan, Italy..
    Sironi, Luigi
    Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy.;Ctr Cardiol Monzino, Milan, Italy..
    Gelosa, Paolo
    Ctr Cardiol Monzino, Milan, Italy..
    Fenofibrate attenuates cardiac and renal alterations in young salt-loaded spontaneously hypertensive stroke-prone rats through mitochondrial protection2018In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 36, no 5, p. 1129-1146Article in journal (Refereed)
    Abstract [en]

    Objectives:The simultaneous presence of cardiac and renal diseases is a pathological condition that leads to increased morbidity and mortality. Several lines of evidence have suggested that lipid dysmetabolism and mitochondrial dysfunction are pathways involved in the pathological processes affecting the heart and kidney. In the salt-loaded spontaneously hypertensive stroke-prone rat (SHRSP), a model of cardiac hypertrophy and nephropathy that shows mitochondrial alterations in the myocardium, we evaluated the cardiorenal effects of fenofibrate, a peroxisome proliferator-activated receptor alpha (PPAR) agonist that acts by modulating mitochondrial and peroxisomal fatty acid oxidation.Methods:Male SHRSPs aged 6-7 weeks were divided in three groups: standard diet (n=6), Japanese diet with vehicle (n=6), and Japanese diet with fenofibrate 150mg/kg/day (n=6) for 5 weeks. Cardiac and renal functions were assessed in vivo by MRI, ultrasonography, and biochemical assays. Mitochondria were investigated by transmission electron microscopy, succinate dehydrogenase (SDH) activity, and gene expression analysis.Results:Fenofibrate attenuated cardiac hypertrophy, as evidenced by histological and MRI analyses, and protected the kidneys, preventing morphological alterations, changes in arterial blood flow velocity, and increases in 24-h proteinuria. Cardiorenal inflammation, oxidative stress, and cellular senescence were also inhibited by fenofibrate. In salt-loaded SHRSPs, we observed severe morphological mitochondrial alterations, reduced SDH activity, and down-regulation of genes regulating mitochondrial fatty-acid oxidation (i.e. PPAR, SIRT3, and Acadm). These changes were counteracted by fenofibrate. In vitro, a direct protective effect of fenofibrate on mitochondrial membrane potential was observed in albumin-stimulated NRK-52E renal tubular epithelial cells.Conclusion:The results suggest that the cardiorenal protective effects of fenofibrate in young male salt-loaded SHRSPs are explained by its capacity to preserve mitochondrial function.

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