The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
Regulation of Macrophage Functions by PPAR-α, PPAR-γ, and LXRs in Mice and Men
Abstract
Peroxisome proliferator-activated receptors (PPARs) and (liver X receptors) LXRs are ligand-activated transcription factors that control lipid and glucose metabolism, as well as the inflammatory response. Because the macrophage plays an important role in host defense and immunoinflammatory pathologies, particular attention has been paid to the role of PPARs and LXRs in the control of macrophage gene expression and function. Research over the last few years has revealed important roles for PPAR-α, PPAR-γ, and LXRs in macrophage inflammation and cholesterol homeostasis with consequences for atherosclerosis development. In this review we will discuss the role of these transcription factors in the control of macrophage activities, with particular attention to species-differences in macrophage function control by PPARs and LXR between rodents and humans.
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Cites
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Cited by
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Macrophages in the Pathogenesis of Atherosclerosis
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Single-cell immune landscape of human atherosclerotic plaques
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Metadata
- Authors
- Rigamonti, E., Chinetti-Gbaguidi, G., & Staels, B.
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2008-06
- Volume
- 28
- Issue
- 6
- Pages
- 1050-1059
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2101395603
- Cited by
- 293
- References
- 19
- FWCI
- 8.07
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Regulation of Macrophage Functions by PPAR-α, PPAR-γ, and LXRs in Mice and Men. https://app.cochat.ai/papers/10.1161/atvbaha.107.158998
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- Rigamonti, E., Chinetti-Gbaguidi, G., & Staels, B. (2008). Regulation of Macrophage Functions by PPAR-α, PPAR-γ, and LXRs in Mice and Men. Arteriosclerosis, Thrombosis, and Vascular Biology. https://doi.org/10.1161/atvbaha.107.158998
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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