The DOI matches its Crossref record; 216 of the 216 references it cites were found in a registry or an index.
Peroxisome proliferator-activated receptors (PPARs): Novel therapeutic targets in renal disease
Open accessAbstract
Peroxisome proliferator-activated receptors (PPARs): Novel therapeutic targets in renal disease. Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily of ligand-dependent transcription factors. PPARs play an important role in the general transcriptional control of numerous cellular processes, including lipid metabolism, glucose homeostasis, cell cycle progression, cell differentiation, inflammation and extracellular matrix remodeling. Three PPAR isoforms, designated PPARalpha, PPARbeta and PPARgamma, have been cloned and are differentially expressed in several tissues including the kidney. PPARalpha primary regulates lipid metabolism and modulates inflammation. PPARalpha is the molecular target of the hypolipidemic fibrates including bezafibrate and clofibrate. PPARbeta participates in embryonic development, implantation and bone formation. PPARgamma is a key factor in adipogenesis and also plays an important role in insulin sensitivity, cell cycle regulation and cell differentiation. Antidiabetic thiazolidinediones (TZDs) such as troglitazone and rosiglitazone are specific ligands of PPARgamma, and this interaction is responsible for the insulin-sensitizing and hypoglycemic effect of these drugs. The kidney has been shown to differentially express all PPAR isoforms. PPARalpha is predominantly expressed in proximal tubules and medullary thick ascending limbs, while PPARgamma is expressed in medullary collecting ducts, pelvic urothelium and glomerular mesangial cells. PPARbeta is ubiquitously expressed at low levels in all segments of nephron. Accumulating data has begun to emerge suggesting physiological and pathophysiological roles of PPARs in several tissues including the kidney. The availability of PPAR-selective agonists and antagonists may provide a new approach to modulate the renal response to diseases including glomerulonephritis, glomerulosclerosis and diabetic nephropathy.
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Cited by
Qiu, Y.-Y., Zhang, J., Zeng, F.-Y., & Zhu, Y. Z. (2023) · Pharmacological Research · doi:10.1016/j.phrs.2023.106786 · Cited by 271
Vallée, A., Lecarpentier, Y., Guillevin, R., & Vallée, J.-N. (2017) · Acta Biochimica et Biophysica Sinica · doi:10.1093/abbs/gmx073 · Cited by 226
PPARα agonist fenofibrate improves diabetic nephropathy in db/db mice
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Self-citationPPARγ ligand attenuates PDGF-induced mesangial cell proliferation: Role of MAP kinase
Ghosh, S. S., Gehr, T. W. B., Ghosh, S., Fakhry, I., Sica, D. A., Lyall, V., & Schoolwerth, A. C. (2003) · Kidney International · doi:10.1046/j.1523-1755.2003.00054.x · Cited by 53
Metadata
- Authors
- Guan, Y., & Breyer, M. D.
- Venue
- Kidney International
- Publisher
- Elsevier BV
- Published
- 2001-07
- Volume
- 60
- Issue
- 1
- Pages
- 14-30
- ISSN
- 0085-2538 (ISSN-L)
- OpenAlex
- W2082460839
- Cited by
- 295
- References
- 216
- FWCI
- 4.45
- Type
- journal article
- Language
- en
- Open access
- bronze
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