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Abolition of mitochondrial substrate-level phosphorylation by itaconic acid produced by LPS-induced Irg1 expression in cells, 2015, Chinopoulos et al

Discussion in 'Health News and Research unrelated to ME/CFS' started by Andy, Apr 2, 2018.

  1. Andy

    Andy Committee Member

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    I think this might be of interest to us but really it's so technical I'm out of my depth.

    What caught my attention was recalling that this recent study claimed that itaconate is an anti-inflammatory metabolite (recent forum thread on the study here) and reading the Wikipedia article that states "However, cells of macrophage lineage have to "pay the price" for making itaconate, and they lose the ability to perform mitochondrial substrate-level phosphorylation.[8]" - the reference is to the study below.

    So my thought process was, if ME is an inflammatory condition, and our body is trying to deal with it by producing itaconate, would this then have a further negative effect that could explain our symptoms. I have no science training so my expectation is that I have misunderstood something and this has no bearing on anything for us at all, but I'm posting it just in case. @Simon M and anybody else, feel free to shoot me down. :)


    Open access at http://www.fasebj.org/doi/10.1096/fj.15-279398
     
    Amw66, Manganus, MarcNotMark and 5 others like this.

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