The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
PPAR γ and the Innate Immune System Mediate the Resolution of Inflammation
Open accessAbstract
The resolution of inflammation is an active and dynamic process, mediated in large part by the innate immune system. Resolution represents not only an increase in anti-inflammatory actions, but also a paradigm shift in immune cell function to restore homeostasis. PPAR γ, a ligand activated transcription factor, has long been studied for its anti-inflammatory actions, but an emerging body of literature is investigating the role of PPAR γ and its ligands (including thiazolidinediones, prostaglandins, and oleanolic acids) in all phases of resolution. PPAR γ can shift production from pro- to anti-inflammatory mediators by neutrophils, platelets, and macrophages. PPAR γ and its ligands further modulate platelet and neutrophil function, decreasing trafficking, promoting neutrophil apoptosis, and preventing platelet-leukocyte interactions. PPAR γ alters macrophage trafficking, increases efferocytosis and phagocytosis, and promotes alternative M2 macrophage activation. There are also roles for this receptor in the adaptive immune response, particularly regarding B cells. These effects contribute towards the attenuation of multiple disease states, including COPD, colitis, Alzheimer’s disease, and obesity in animal models. Finally, novel specialized proresolving mediators—eicosanoids with critical roles in resolution—may act through PPAR γ modulation to promote resolution, providing another exciting area of therapeutic potential for this receptor.
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Cites
Resolving inflammation: dual anti-inflammatory and pro-resolution lipid mediators
Serhan, C. N., Chiang, N., & Van Dyke, T. E. (2008) · Nature Reviews Immunology · doi:10.1038/nri2294 · Cited by 2,932
Kliewer, S. A., Sundseth, S. S., Jones, S. A., Brown, P. J., Wisely, G. B., Koble, C. S., Devchand, P., Wahli, W., Willson, T. M., Lenhard, J. M., et al. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.9.4318 · Cited by 2,164
Macrophage-specific PPARγ controls alternative activation and improves insulin resistance
Odegaard, J. I., Ricardo-Gonzalez, R. R., Goforth, M. H., Morel, C. R., Subramanian, V., Mukundan, L., Eagle, A. R., Vats, D., Brombacher, F., Ferrante, A. W., et al. (2007) · Nature · doi:10.1038/nature05894 · Cited by 2,107 · cited 2×
“PPAR𝛾 ligands play a particularly strong role in M2 polarization in the neural system.”
BackgroundMethodMolecular recognition of fatty acids by peroxisome proliferator-activated receptors
Xu, H. E., Lambert, M. H., Montana, V. G., Parks, D. J., Blanchard, S. G., Brown, P. J., Sternbach, D. D., Lehmann, J. M., Wisely, G. B., Willson, T. M., et al. (1999) · Molecular Cell · doi:10.1016/s1097-2765(00)80467-0 · Cited by 1,169
Mandrekar-Colucci, S., Karlo, J. C., & Landreth, G. E. (2012) · The Journal of Neuroscience · doi:10.1523/jneurosci.5268-11.2012 · Cited by 355 · cited 1×
“Pioglitazone promoted a shift from M1 to M2 macrophages and enhanced Aβ amyloid phagocytosis in the brain [74].”
BackgroundYamanaka, M., Ishikawa, T., Griep, A., Axt, D., Kummer, M. P., & Heneka, M. T. (2012) · The Journal of Neuroscience · doi:10.1523/jneurosci.1569-12.2012 · Cited by 326
Zhao, Y., Calon, F., Julien, C., Winkler, J. W., Petasis, N. A., Lukiw, W. J., & Bazan, N. G. (2011) · PLoS ONE · doi:10.1371/journal.pone.0015816 · Cited by 243
Macrophage PPARγ and impaired wound healing in type 2 diabetes
Mirza, R. E., Fang, M. M., Novak, M. L., Urao, N., Sui, A., Ennis, W. J., & Koh, T. J. (2015) · The Journal of Pathology · doi:10.1002/path.4548 · Cited by 177
Fernandez-Boyanapalli, R., Frasch, S. C., Riches, D. W. H., Vandivier, R. W., Henson, P. M., & Bratton, D. L. (2010) · Blood · doi:10.1182/blood-2010-02-272005 · Cited by 98
Nuclear receptors in neurodegenerative diseases
Skerrett, R., Malm, T., & Landreth, G. (2014) · Neurobiology of Disease · doi:10.1016/j.nbd.2014.05.019 · Cited by 94
Cited by
Postler, T. S., & Ghosh, S. (2017) · Cell Metabolism · doi:10.1016/j.cmet.2017.05.008 · Cited by 876
“Given the anti-inflammatory effects described for PPAR-g, future studies are likely to further explore this topic (Croasdell et al., 2015).”
BackgroundMechanisms and Mitochondrial Redox Signaling in Photobiomodulation
Hamblin, M. R. (2018) · Photochemistry and Photobiology · doi:10.1111/php.12864 · Cited by 820
Consideration of pathways for immunotoxicity of per-and polyfluoroalkyl substances (PFAS)
Ehrlich, V., Bil, W., Vandebriel, R., Granum, B., Luijten, M., Lindeman, B., Grandjean, P., Kaiser, A.-M., Hauzenberger, I., Hartmann, C., et al. (2023) · Environmental Health · doi:10.1186/s12940-022-00958-5 · Cited by 318
Leukocyte trafficking to the lungs and beyond: lessons from influenza for COVID-19
Alon, R., Sportiello, M., Kozlovski, S., Kumar, A., Reilly, E. C., Zarbock, A., Garbi, N., & Topham, D. J. (2021) · Nature Reviews Immunology · doi:10.1038/s41577-020-00470-2 · Cited by 197
Yang, H.-T., Chen, J.-W., Rathod, J., Jiang, Y.-Z., Tsai, P.-J., Hung, Y.-P., Ko, W.-C., Paredes-Sabja, D., & Huang, I.-H. (2018) · Frontiers in Microbiology · doi:10.3389/fmicb.2017.02635 · Cited by 117
Metadata
- Authors
- Croasdell, A., Duffney, P. F., Kim, N., Lacy, S. H., Sime, P. J., & Phipps, R. P.
- Venue
- PPAR Research
- Publisher
- Wiley
- Published
- 2015
- Volume
- 2015
- Pages
- 1-20
- ISSN
- 1687-4757 (ISSN-L)
- 1687-4765
- OpenAlex
- W2185633290
- Cited by
- 239
- References
- 11
- FWCI
- 6.82
- Type
- journal article
- Language
- en
- Open access
- gold
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- Croasdell, A., Duffney, P. F., Kim, N., Lacy, S. H., Sime, P. J., & Phipps, R. P. (2015). PPAR γ and the Innate Immune System Mediate the Resolution of Inflammation. PPAR Research. https://doi.org/10.1155/2015/549691
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.