ArticleInflammatory bowel diseases2025
Mitochondrial Dysfunction: Unraveling the Elusive Biology Behind Anti-TNF Response During Ulcerative Colitis.
Article in Inflammatory bowel diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Mitochondrial Dysfunction in Ulcerative Colitis: Pathogenic Mechanisms and Novel Therapeutics.Journal of biochemical and molecular toxicology · 2026Review
- Resistance Training Complements Anti-TNF Therapy in DSS-Induced Colitis by Improving Skeletal Muscle Inflammatory and Mitochondrial Gene Signatures.Current issues in molecular biology · 2026Article
- Short-term caloric restriction partially reprograms immune and microbial networks during acute DSS-induced colitis.Genes & nutrition · 2026Article
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Authors and funding
18 authors.
Funding
Abstract
backgroundRecent studies hint at mitochondrial genes influencing UC patient response to anti-TNF treatment. We evaluated this hypothesis by following a targeted strategy to identify gene expression that captures the relationship between mitochondrial dysregulation and response to treatment. Our objective was to initially examine this relationship in colon samples and subsequently assess whether the resulting signal persists in the bloodstream.
methodsWe analyzed the transcriptome of colon samples from an anti-TNF-treated murine model characterized by impaired mitochondrial activity and treatment resistance. We then transferred the findings that linked mitochondrial dysfunction and compromised treatment response to an anti-TNF-treated UC human cohort. We next matched differential expression in the blood using monocytes from the peripheral blood of controls and IBD patients, and we evaluated a classification process at baseline with whole blood samples from UC patients.
resultsIn human colon samples, the derived gene set from the murine model showed differential expression, primarily enriched metabolic pathways, and exhibited similar classification capacity as genes enriching inflammatory pathways. Moreover, the evaluation of the classification signal using blood samples from UC patients at baseline highlighted the involvement of mitochondrial homeostasis in treatment response.
conclusionsOur results highlight the involvement of metabolic pathways and mitochondrial homeostasis in determining treatment response and their ability to provide promising classification signals with detection levels in both the colon and the bloodstream.
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