000 | 01546 am a22002173u 4500 | ||
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042 | _adc | ||
100 | 1 | 0 |
_aCasey, Alva M. _eauthor _93172 |
700 | 1 | 0 |
_aMurphy, Michael P. _eauthor _93173 |
245 | 0 | 0 | _aUncovering the source of mitochondrial superoxide in pro-inflammatory macrophages: Insights from immunometabolism |
260 | _c2022-10-01. | ||
500 | _a/pmc/articles/PMC7614207/ | ||
500 | _a/pubmed/35792320 | ||
520 | _aMitochondrial-derived reactive oxygen species are important as antimicrobial agents and redox signals in pro-inflammatory macrophages. Macrophages produce superoxide in response to the TLR4 ligand LPS. However, the mechanism of LPS-induced superoxide generation is not fully understood. Superoxide is produced at complex I and complex III of the electron transport chain. Production of superoxide at either of these sites is highly dependent on the metabolic state of the cell which is dramatically altered by TLR4-induced metabolic reprogramming. This review will outline how metabolism impacts superoxide production in LPS-activated macrophages downstream of TLR4 signalling and address outstanding questions in this field. | ||
540 | _a | ||
540 | _ahttps://creativecommons.org/licenses/by/4.0/This work is licensed under a CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/) International license. | ||
546 | _aen | ||
690 | _aArticle | ||
655 | 7 |
_aText _2local |
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786 | 0 | _nBiochim Biophys Acta Mol Basis Dis | |
856 | 4 | 1 |
_uhttp://dx.doi.org/10.1016/j.bbadis.2022.166481 _zConnect to this object online. |
999 |
_c2252 _d2252 |