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Review
. 2022 Mar 4:13:832732.
doi: 10.3389/fphar.2022.832732. eCollection 2022.

The Role of Peroxisome Proliferator-Activated Receptors in Kidney Diseases

Affiliations
Review

The Role of Peroxisome Proliferator-Activated Receptors in Kidney Diseases

Jianjun Gao et al. Front Pharmacol. .

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.

Keywords: acute kidney injury; chronic kidney disease; diabetic nephropathy; kidney disease; peroxisome proliferator-activated receptors.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Structure and molecular mechanism of action of peroxisome proliferator-activated receptors.

References

    1. Arany Z., He H., Lin J., Hoyer K., Handschin C., Toka O., et al. (2005). Transcriptional Coactivator PGC-1 Alpha Controls the Energy State and Contractile Function of Cardiac Muscle. Cell Metab 1, 259–271. 10.1016/j.cmet.2005.03.002 - DOI - PubMed
    1. Arora M. K., Reddy K., Balakumar P. (2010). The Low Dose Combination of Fenofibrate and Rosiglitazone Halts the Progression of Diabetes-Induced Experimental Nephropathy. Eur. J. Pharmacol. 636, 137–144. 10.1016/j.ejphar.2010.03.002 - DOI - PubMed
    1. Bae E. H., Kim I. J., Ma S. K., Kim S. W. (2010). Rosiglitazone Prevents the Progression of Renal Injury in DOCA-Salt Hypertensive Rats. Hypertens. Res. 33, 255–262. 10.1038/hr.2009.217 - DOI - PubMed
    1. Bakris G., Viberti G., Weston W. M., Heise M., Porter L. E., Freed M. I. (2003). Rosiglitazone Reduces Urinary Albumin Excretion in Type II Diabetes. J. Hum. Hypertens. 17, 7–12. 10.1038/sj.jhh.1001444 - DOI - PubMed
    1. Baud L., Letavernier E. (2007). PPARalpha Contributes to Tubular protection. J. Am. Soc. Nephrol. 18, 3017–3018. 10.1681/ASN.2007091036 - DOI - PubMed

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