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- W2162280260 abstract "See article by Planavila et al. [6] (pages 832–841) in this issue. In the normal adult heart, plasticity of ATP production is provided by coordinated changes in the expression of genes involved in cellular fatty acid (FA) utilization and glucose oxidation. The phenotypes of acquired forms of heart failure in human and animal models are associated with energy substrate changes accompanying a reduced mitochondrial FA oxidative capacity and a shift to glucose metabolism, resembling the fetal metabolic program [1]. High glucose conditions, initially serving as a protective response to support contractile function, stimulate the production of angiotensin II (Ang II), a known pathological modulator of cardiac remodeling [2].Peroxisome proliferator-activated receptors (PPARs) are gene regulatory systems that regulate the transcription of an array of genes involved in cellular fatty acid utilization pathways. PPARs are ligand-dependent transcription factors belonging to the nuclear receptor superfamily. They are designed to rapidly respond to fluctuating substrate and metabolic intermediates. They regulate pathways involved in FA utilization upstream to the transcriptional regulatory network including nuclear respiratory factors 1 and 2 and mitochondrial transcription factor A [3]. PPARs have 3 isoforms, α, β/δ, and γ, that regulate lipid and glucose metabolism, participate in the regulation … *Corresponding author. Tel.: +1 513 558 2374; fax: +1 513 558 1778. Email address: petrasnn{at}email.uc.edu" @default.
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- W2162280260 date "2005-03-01" @default.
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- W2162280260 title "Peroxisome proliferator-activated receptor ?/?: a new antihypertrophic drug target?" @default.
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- W2162280260 doi "https://doi.org/10.1016/j.cardiores.2005.01.009" @default.
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