Peroxisome proliferator-activated receptors and renal diseases

Wu, Jing; Zhang, Dongjuan; Huo, Ming; Zhang, Xiaoyan; Pu, Dan; Guan, Youfei

doi:10.2741/3291

Cited by 24 publications

(21 citation statements)

References 105 publications

(97 reference statements)

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“…PPARs heterodimerize with the retinoid X receptor (RXR) and bind to PPAR responsive element (PPRE) in the regulatory region of target genes that function in diverse biological processes, such as lipid metabolism, adipogenesis, insulin sensitivity, immune response, and cell growth and differentiation [1, 2]. PPARs also participate in the pathogenesis of a cluster of human diseases, for example, metabolic syndrome that includes insulin resistance, glucose intolerance, obesity, dyslipidemia, hypertension, atherosclerosis, and microalbuminuria [3–6].…”

Section: Introductionmentioning

confidence: 99%

PPARs Integrate the Mammalian Clock and Energy Metabolism

2014

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Peroxisome proliferator-activated receptors (PPARs) are a group of nuclear receptors that function as transcription factors regulating the expression of numerous target genes. PPARs play an essential role in various physiological and pathological processes, especially in energy metabolism. It has long been known that metabolism and circadian clocks are tightly intertwined. However, the mechanism of how they influence each other is not fully understood. Recently, all three PPAR isoforms were found to be rhythmically expressed in given mouse tissues. Among them, PPARα and PPARγ are direct regulators of core clock components, Bmal1 and Rev-erbα, and, conversely, PPARα is also a direct Bmal1 target gene. More importantly, recent studies using knockout mice revealed that all PPARs exert given functions in a circadian manner. These findings demonstrated a novel role of PPARs as regulators in correlating circadian rhythm and metabolism. In this review, we summarize advances in our understanding of PPARs in circadian regulation.

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Section: Introductionmentioning

confidence: 99%

PPARs Integrate the Mammalian Clock and Energy Metabolism

2014

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“…Fenofibrate is a classic PPARα agonist. It has been demonstrated in multiple animal studies that fenofibrate reduces albuminuria in patients with diabetes [25,61,87] . In addition to reducing albuminuria, fenofibrate has been reported to ameliorate hyperglycemia [88,89] .…”

Section: Metabolic Nuclear Receptors: Great Promise?mentioning

confidence: 99%

“…Activation of PPARγ modulates the transcription of a number of insulin-responsive genes involved in the control of glucose and lipid metabolism. PPARα and PPARγ modulate energy utilization in the kidney by regulating FAO [61] . Activation of PPARα can stimulate FA β-oxidation, which can reduce the lipid content, and exerts renoprotective effects.…”

Section: Metabolic Nuclear Receptorsmentioning

confidence: 99%

Crosstalk of Hyperglycemia and Dyslipidemia in Diabetic Kidney Disease

Cao

et al. 2017

Kidney Dis

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Background: Diabetic kidney disease (DKD) is defined by the functional, structural, and clinical abnormalities of the kidney that are caused by diabetes. Summary: One-third of both type 1 diabetes and type 2 diabetes patients suffer from DKD, which is the leading cause of end-stage renal disease, and is also associated with cardiovascular disease and high public health care costs. Serum glucose level and lipid level are key factors in the pathogenesis of DKD and are modifiable. The goal of this review is to provide an update on the roles of glucose and lipid metabolism in DKD and their crosstalk at the molecular level. We will further discuss the recent advances regarding metabolic nuclear receptors in glucose-lipid crosstalk, which may provide new potential therapeutic targets for DKD. Key Message: AMPK, SREBP-1, and some metabolic hormone receptors including liver X receptors, farnesoid X receptors, and peroxisome proliferator-activated receptors mediate the crosstalk of hyperglycemia and dyslipidemia in diabetic kidney disease and might be potential treatment candidates.

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“…The RXRA/PPARA heterodimer is required for PPRA transcriptional activity on fatty acid oxidation genes (71). PPARA itself is a major regulator of lipid metabolism, particularly fatty acid utilization (72), and PPARA inhibition results in hypertriglyceridemia (73). Fatty acid oxidation capacity is decreased at the transcript level in native kidneys with fibrosis (70).…”

Section: L I N I C a L M E D I C I N Ementioning

confidence: 99%