Abstract
Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily of ligand-activated transcription factors. Accumulating evidence suggests that PPARs may play an important role in the pathogenesis of kidney disease. All three members of the PPAR subfamily, PPARα, PPARβ/δ, and PPARγ, have been implicated in many renal pathophysiological conditions, including acute kidney injury, diabetic nephropathy, and chronic kidney disease, among others. Emerging data suggest that PPARs may be potential therapeutic targets for renal disease. This article reviews the physiological roles of PPARs in the kidney and discusses the therapeutic utility of PPAR agonists in the treatment of kidney disease.
Highlights
Peroxisome proliferator-activated receptors (PPARs), a group of nuclear hormone receptors, consist of threeisotypes, i.e., PPARα, PPARβ/δ, and PPARγ (Xi et al, 2020)
PPARα was shown to be downregulated in aggressive mouse models of autosomal dominant polycystic kidney disease (ADPKD) and primary human ADPKD cells, suggesting that decreased PPARα function may underlie the impaired fatty acid oxidation (FAO) and oxidative phosphorylation in ADPKD (Hajarnis et al, 2017; Lakhia et al, 2018)
Treatment with fenofibrate increased PPARα expression, prevented high-fat diet (HFD)-induced renal lipotoxicity, reduced oxidative stress and lipid accumulation in the glomeruli, and prevented the development of albuminuria and glomerular fibrosis (Tanaka et al, 2011; Chung et al, 2012). These findings suggest that PPARα may be a novel therapeutic target for the treatment of kidney disease
Summary
Peroxisome proliferator-activated receptors (PPARs), a group of nuclear hormone receptors, consist of threeisotypes, i.e., PPARα, PPARβ/δ, and PPARγ (Xi et al, 2020). PPARs can regulate gene transcription in either ligand-dependent or -independent manner. The target genes are critical for fatty acid oxidation (FAO) and transportation, glucose metabolism, adipogenesis, cholesterol transportation and biosynthesis, apoptosis, and the inflammatory response (Tyagi et al, 2011; Derosa et al, 2018). Numerous studies employing experimental and clinical models have shown that PPARs play important roles in lipid metabolism and energy homeostasis in the kidney (TovarPalacio et al, 2012; Corrales et al, 2018) (Table 1). This review focuses on the roles of PPARs in renal metabolism as well as therapeutic strategies targeting the activation of PPARs in kidney disease
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