The kynurenine pathway in chronic diseases: a compensatory mechanism or a driving force?

Niklas Joisten*, Jorge L. Ruas, Nady Braidy, Gilles J. Guillemin, Philipp Zimmer

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

13 Citations (Scopus)


The kynurenine (KYN) pathway (KP) of tryptophan (TRP) metabolism is dysregulated in inflammation-driven pathologies including oncological and brain diseases [e.g., multiple sclerosis (MS), depression] and thus is a promising therapeutic target. Both pathological and compensatory mechanisms underlie disease-associated KP activation. There is growing evidence for bioenergetic roles of certain KP metabolites such as kynurenic acid (KA), or quinolinic acid (QA) as an NAD+ precursor, which may explain its frequently observed ‘pathological’ overactivation. Disease- and tissue-specific aspects, negative feedback on inflammatory signals, and the balance of downstream metabolites are likely to be decisive factors in the interpretation of an imbalanced KP. Therapeutic strategies should consider the compensatory actions and bioenergetic roles of KP metabolites to successfully design future theragnostic approaches aimed at attenuating disease progression.

Original languageEnglish
Pages (from-to)946-954
Number of pages9
JournalTrends in Molecular Medicine
Issue number10
Publication statusPublished - Oct 2021


  • bioenergetics
  • inflammation
  • kynurenines
  • metabolism
  • tryptophan


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