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@ARTICLE{He:164641,
author = {He, Wei and Henne, Antonia and Lauterbach, Mario and
Geißmar, Eike and Nikolka, Fabian and Kho, Celia and Heinz,
Alexander and Dostert, Catherine and Grusdat, Melanie and
Cordes, Thekla and Härm, Janika and Goldmann, Oliver and
Ewen, Anouk and Verschueren, Charlène and Blay-Cadanet,
Julia and Geffers, Robert and Garritsen, Hendrikus and
Kneiling, Manfred and Holm, Christian K and Metallo,
Christian M and Medina, Eva and Abdullah, Zeinab and Latz,
Eicke and Brenner, Dirk and Hiller, Karsten},
title = {{M}esaconate is synthesized from itaconate and exerts
immunomodulatory effects in macrophages.},
journal = {Nature metabolism},
volume = {4},
number = {5},
issn = {2522-5812},
address = {[London]},
publisher = {Springer Nature},
reportid = {DZNE-2022-01171},
pages = {524 - 533},
year = {2022},
abstract = {Since its discovery in inflammatory macrophages, itaconate
has attracted much attention due to its antimicrobial and
immunomodulatory activity1-3. However, instead of
investigating itaconate itself, most studies used
derivatized forms of itaconate and thus the role of
non-derivatized itaconate needs to be scrutinized.
Mesaconate, a metabolite structurally very close to
itaconate, has never been implicated in mammalian cells.
Here we show that mesaconate is synthesized in inflammatory
macrophages from itaconate. We find that both,
non-derivatized itaconate and mesaconate dampen the
glycolytic activity to a similar extent, whereas only
itaconate is able to repress tricarboxylic acid cycle
activity and cellular respiration. In contrast to itaconate,
mesaconate does not inhibit succinate dehydrogenase. Despite
their distinct impact on metabolism, both metabolites exert
similar immunomodulatory effects in pro-inflammatory
macrophages, specifically a reduction of interleukin (IL)-6
and IL-12 secretion and an increase of CXCL10 production in
a manner that is independent of NRF2 and ATF3. We show that
a treatment with neither mesaconate nor itaconate impairs
IL-1β secretion and inflammasome activation. In summary,
our results identify mesaconate as an immunomodulatory
metabolite in macrophages, which interferes to a lesser
extent with cellular metabolism than itaconate.},
keywords = {Animals / Inflammasomes / Macrophages: drug effects /
Macrophages: metabolism / Mice / RAW 264.7 Cells /
Succinates: metabolism / Succinates: pharmacology /
Inflammasomes (NLM Chemicals) / Succinates (NLM Chemicals) /
itaconic acid (NLM Chemicals)},
cin = {AG Latz ; AG Latz},
ddc = {610},
cid = {I:(DE-2719)1013024},
pnm = {351 - Brain Function (POF4-351)},
pid = {G:(DE-HGF)POF4-351},
typ = {PUB:(DE-HGF)16},
pmc = {pmc:PMC9744384},
pubmed = {pmid:35655024},
doi = {10.1038/s42255-022-00565-1},
url = {https://pub.dzne.de/record/164641},
}