ReviewVirulence2026
Itaconate as an immunometabolic hub in host-pathogen interactions: Mechanisms, resistance, and therapeutic opportunities.
Review in Virulence, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Produced by IRG1 in macrophages, itaconate has emerged as an immunometabolic hub at the host-pathogen interface. This review integrates itaconate's roles in antimicrobial defense. We first examine how itaconate inhibits pathogen metabolism by targeting key enzymes including isocitrate lyase, fructose-bisphosphate aldolase, and inosine monophosphate dehydrogenase. Beyond direct inhibition, itaconate reprograms host immunity through SDH suppression, Nrf2 activation, ATF3 induction, and context-dependent NLRP3 regulation, and promotes lysosomal biogenesis via TFEB. Conversely, pathogens have evolved counter strategies including enzymatic degradation, biofilm formation, and immune microenvironment remodeling. We also summarize preclinical evidence supporting itaconate and derivatives' therapeutic potential for infection-associated conditions. Finally, we appraise theoretical gaps and methodological challenges, offering guidance for future investigation in this rapidly advancing field.
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Registered trials
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