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Review
. 2017 May;13(3):279-296.
doi: 10.2217/fca-2017-0019. Epub 2017 Jun 5.

PPARs: regulators of metabolism and as therapeutic targets in cardiovascular disease. Part II: PPAR-β/δ and PPAR-γ

Lu Han  1   2 , Wen-Jun Shen  1   2 , Stefanie Bittner  1 , Fredric B Kraemer  1   2 , Salman Azhar  1   2
Affiliations
Review

PPARs: regulators of metabolism and as therapeutic targets in cardiovascular disease. Part II: PPAR-β/δ and PPAR-γ

Lu Han et al. Future Cardiol. 2017 May.

Abstract

The PPARs are a subfamily of three ligand-inducible transcription factors, which belong to the superfamily of nuclear hormone receptors. In mammals, the PPAR subfamily consists of three members: PPAR-α, PPAR-β/δ and PPAR-γ. PPARs control the expression of a large number of genes involved in metabolic homeostasis, lipid, glucose and energy metabolism, adipogenesis and inflammation. PPARs regulate a large number of metabolic pathways that are implicated in the pathogenesis of metabolic diseases such as metabolic syndrome, Type 2 diabetes mellitus, nonalcoholic fatty liver disease and cardiovascular disease. The aim of this review is to provide up-to-date information about the biochemical and metabolic actions of PPAR-β/δ and PPAR-γ, the therapeutic potential of their agonists currently under clinical development and the cardiovascular disease outcome of clinical trials of PPAR-γ agonists, pioglitazone and rosiglitazone.

Keywords: NAFLD; PPAR-β/δ agonist; PPAR-γ agonist; Type 2 diabetes; cardiovascular disease; hyperglycemia; hyperinsulinemia; lipid and glucose metabolism; metabolic syndrome.

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Conflict of interest statement

Financial & competing interests disclosure

This work was supported by the Office of Research and Development, Medical Service, Department of Veterans Affairs, and grants from the NIH (HL033881 and HL092473). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

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