Peroxisome proliferator-activated receptors (PPARs): nuclear receptors at the crossroads between lipid metabolism and inflammation
Abstract
Peroxisome proliferator-activated (PPARs) are ligand-activated transcription factors belonging to the nuclear receptor family. PPARs function as regulators of lipid and lipoprotein metabolism and glucose homeostasis and influence cellular proliferation, differentiation and apoptosis. PPARalpha is highly expressed in tissues such as liver, muscle, kidney and heart, where it stimulates the beta-oxidative degradation of fatty acids. PPARgamma is predominantly expressed in intestine and adipose tissue. PPARgamma triggers adipocyte differentiation and promotes lipid storage. The hypolipidemic fibrates and the antidiabetic glitazones are synthetic ligands for PPARalpha and PPARgamma, respectively. Furthermore, fatty acids and eicosanoids are natural PPAR ligands: PPARalpha is activated by leukotriene B4, whereas prostaglandin J2 is a PPARgamma ligand. These observations suggested a potential role for PPARs not only in metabolic but also in inflammation control. The first evidence for a role of PPARalpha in inflammation control came from the demonstration that PPARalpha deficient mice display a prolonged response to inflammatory stimuli. It was suggested that PPARalpha deficiency results in a reduced beta-oxidative degradation of these inflammatory fatty acid derivatives. More recently, PPAR activators were shown to inhibit the activation of inflammatory response genes (such as IL-2, IL-6, IL-8, TNFalpha and metalloproteases) by negatively interfering with the NF- kappaB, STAT and AP-1 signalling pathways. PPAR activators exert these anti-inflammatory activities in different immunological and vascular wall cell types such as monocyte/macrophages, endothelial, epithelial and smooth muscle cells in which PPARs are expressed. These recent findings indicate a modulatory role for PPARs in the control of the inflammatory response with potential therapeutic applications in inflammation-related diseases, such as atherosclerosis and inflammatory bowel disease.
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PPARs are nuclear hormone receptors that respond to binding of endogenous fatty acids and fatty acid derivatives such as eicosanoids, by regulating expression of genes within diverse cellular pathways including lipid metabolism and inflammation.
“PPARs are nuclear hormone receptors that respond to binding of endogenous fatty acids and fatty acid derivatives such as eicosanoids, by regulating expression of genes within diverse cellular pathways including lipid metabolism and inflammation (Kliewer et al., 1997; Chinetti et al., 2000).”
From The cell biology of the retinal pigment epithelium (2020) · cites this paper as Chinetti et al., 2000
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References 74 · Cited by 954
- Authors
- Chinetti, G., Fruchart, J.-C., & Staels, B.
- Affiliations
- Inserm (FR)
- Venue
- Inflammation Research
- Published
- 2000-10-01
- Volume
- 49
- Issue
- 10
- Pages
- 497-505
- ISSN
- 1023-3830 (ISSN-L)
- 1420-908X
- OpenAlex
- W1978380407
- Cited by
- 954
- References
- 74
- Citations by year
- 2026: 14 · 2025: 25 · 2024: 25 · 2023: 30 · 2022: 28 · 2021: 28 · 2020: 40 · 2019: 29 · 2018: 34 · 2017: 32 · 2016: 27 · 2015: 32 · 2014: 43 · 2013: 36 · 2012: 42
- FWCI
- 11.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Inflammation Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
- Keywords
- peroxisome proliferator-activated receptors, PPARα, PPARγ, nuclear receptors, lipid metabolism, glucose homeostasis, fatty acid beta-oxidation, adipogenesis, fibrates, thiazolidinediones, leukotriene B4, prostaglandin J2, inflammation, NF-κB signaling, STAT signalling, atherosclerosis, inflammatory bowel disease, anti-inflammatory therapy
- MeSH terms
- Acute-Phase Proteins, Animals, Arteriosclerosis, Gene Expression Regulation, Humans, Inflammation, Macrophages, Transcription Factors, Inflammatory Bowel Diseases, Cytokines, Receptors, Cytoplasmic and Nuclear, Lipid Metabolism
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