The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
PKM2-dependent glycolysis promotes NLRP3 and AIM2 inflammasome activation
Open accessAbstract
Sepsis, severe sepsis and septic shock are the main cause of mortality in non-cardiac intensive care units. Immunometabolism has been linked to sepsis; however, the precise mechanism by which metabolic reprogramming regulates the inflammatory response is unclear. Here we show that aerobic glycolysis contributes to sepsis by modulating inflammasome activation in macrophages. PKM2-mediated glycolysis promotes inflammasome activation by modulating EIF2AK2 phosphorylation in macrophages. Pharmacological and genetic inhibition of PKM2 or EIF2AK2 attenuates NLRP3 and AIM2 inflammasomes activation, and consequently suppresses the release of IL-1β, IL-18 and HMGB1 by macrophages. Pharmacological inhibition of the PKM2–EIF2AK2 pathway protects mice from lethal endotoxemia and polymicrobial sepsis. Moreover, conditional knockout of PKM2 in myeloid cells protects mice from septic death induced by NLRP3 and AIM2 inflammasome activation. These findings define an important role of PKM2 in immunometabolism and guide future development of therapeutic strategies to treat sepsis.
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Cites
1 retracted
UCP2-induced fatty acid synthase promotes NLRP3 inflammasome activation during sepsis
Moon, J.-S., Lee, S., Park, M.-A., Siempos, I. I., Haslip, M., Lee, P. J., Yun, M., Kim, C. K., Howrylak, J., Ryter, S. W., et al. (2015) · Journal of Clinical Investigation · doi:10.1172/jci78253 · Cited by 238
RetractedSuccinate is an inflammatory signal that induces IL-1β through HIF-1α
Tannahill, G. M., Curtis, A. M., Adamik, J., Palsson-McDermott, E. M., McGettrick, A. F., Goel, G., Frezza, C., Bernard, N. J., Kelly, B., Foley, N. H., et al. (2013) · Nature · doi:10.1038/nature11986 · Cited by 4,176
Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling
Kayagaki, N., Stowe, I. B., Lee, B. L., O’Rourke, K., Anderson, K., Warming, S., Cuellar, T., Haley, B., Roose-Girma, M., Phung, Q. T., et al. (2015) · Nature · doi:10.1038/nature15541 · Cited by 3,686
Activation and regulation of the inflammasomes
Latz, E., Xiao, T. S., & Stutz, A. (2013) · Nature Reviews Immunology · doi:10.1038/nri3452 · Cited by 2,884
Inflammatory caspases are innate immune receptors for intracellular LPS
Shi, J., Zhao, Y., Wang, Y., Gao, W., Ding, J., Li, P., Hu, L., & Shao, F. (2014) · Nature · doi:10.1038/nature13683 · Cited by 2,285
Shi, L. Z., Wang, R., Huang, G., Vogel, P., Neale, G., Green, D. R., & Chi, H. (2011) · Journal of Experimental Medicine · doi:10.1084/jem.20110278 · Cited by 1,803
Control of TH17/Treg Balance by Hypoxia-Inducible Factor 1
Dang, E. V., Barbi, J., Yang, H.-Y., Jinasena, D., Yu, H., Zheng, Y., Bordman, Z., Fu, J., Kim, Y., Yen, H.-R., et al. (2011) · Cell · doi:10.1016/j.cell.2011.07.033 · Cited by 1,595
Palsson-McDermott, E. M., Curtis, A. M., Goel, G., Lauterbach, M. A. R., Sheedy, F. J., Gleeson, L. E., van den Bosch, M. W. M., Quinn, S. R., Domingo-Fernandez, R., Johnston, D. G. W., et al. (2015) · Cell Metabolism · doi:10.1016/j.cmet.2014.12.005 · Cited by 1,397
Self-citation
Cited by
Inflammation, metaflammation and immunometabolic disorders
Hotamisligil, G. S. (2017) · Nature · doi:10.1038/nature21363 · Cited by 2,570
Macrophage Immunometabolism: Where Are We (Going)?
Van den Bossche, J., O’Neill, L. A., & Menon, D. (2017) · Trends in Immunology · doi:10.1016/j.it.2017.03.001 · Cited by 1,163
NLRP3 Inflammasome and the IL-1 Pathway in Atherosclerosis
Grebe, A., Hoss, F., & Latz, E. (2018) · Circulation Research · doi:10.1161/circresaha.118.311362 · Cited by 926
Pan, R.-Y., He, L., Zhang, J., Liu, X., Liao, Y., Gao, J., Liao, Y., Yan, Y., Li, Q., Zhou, X., et al. (2022) · Cell Metabolism · doi:10.1016/j.cmet.2022.02.013 · Cited by 862
Lee (2019) · doi:10.1038/s12276-019-0299-y · Cited by 635
Metadata
- Authors
- Xie, M., Yu, Y., Kang, R., Zhu, S., Yang, L., Zeng, L., Sun, X., Yang, M., Billiar, T. R., Wang, H., Cao, L., Jiang, J., & Tang, D.
- Venue
- Nature Communications
- Published
- 2016-10-25
- Volume
- 7
- Issue
- 1
- Pages
- 13280-13280
- ISSN
- 2041-1723 (ISSN-L)
- OpenAlex
- W2532112957
- Cited by
- 568
- References
- 8
- FWCI
- 14.14
- Type
- journal article
- Language
- en
- Open access
- gold
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- Xie, M., Yu, Y., Kang, R., Zhu, S., Yang, L., Zeng, L., Sun, X., Yang, M., Billiar, T. R., Wang, H., Cao, L., Jiang, J., & Tang, D. (2016). PKM2-dependent glycolysis promotes NLRP3 and AIM2 inflammasome activation. Nature Communications. https://doi.org/10.1038/ncomms13280
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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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