ArticleJournal of inflammation research2025
Mitochondrial Dysfunction and Reduced TCA Cycle Metabolite Levels in Inflammatory Bowel Disease Patients.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Proteomic Analysis of Dairy Cows with Persistent Subclinical Hypocalcemia.Animals : an open access journal from MDPI · 2026Article
- TET Enzymes as Epigenetic Integrators in Intestinal Immunity, Inflammation, and Disease.Journal of personalized medicine · 2026Review
- Mitochondrial Dysfunction in Ulcerative Colitis: Pathogenic Mechanisms and Novel Therapeutics.Journal of biochemical and molecular toxicology · 2026Review
- Dietary PhIP Exposure Induces Intestinal Barrier Injury in Zebrafish Involving Proteobacteria-Associated Dysbiosis and Metabolic Remodeling.Foods (Basel, Switzerland) · 2026Article
- 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
- Inorganic nitrogen metabolic reprogramming of the gut microbiome drives fecal microbiota transplantation in ulcerative colitis.Nature communications · 2026Article
- Dysfunction of mitochondria in intestinal epithelial cells: a key player in the pathogenesis of inflammatory bowel diseases.Gastroenterology report · 2026Review
- The Interplay of One-Carbon Metabolism, Mitochondrial Function, and Developmental Programming in Ruminant Livestock.Journal of developmental biology · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Inflammatory bowel disease (IBD) mainly includes ulcerative colitis (UC) and Crohn's disease (CD). These diseases are classified as chronic and recurrent inflammatory diseases affecting the digestive tract. An energy deficiency in intestinal cells is believed to be associated with IBD pathology. Methods: Our study investigated the bioenergetic functionality of mitochondria using the plasma of patients with CD and UC by determining the concentration of intermediates of the tricarboxylic acid cycle (TCA), such as acetyl coenzyme A, succinate, fumarate, α-ketoglutarate, NADH2, IDH2, Cytochrome C Oxidase, Cytochrome C Reductase, and ATP. Results: Our results show an imbalance in mitochondrial homeostasis and bioenergetics, demonstrated by reduced activity of respiratory complexes and reduced production of TCA intermediates in the plasma of patients with CD and UC. In the group of patients with CD, treatment with corticosteroids had a significant positive effect, as significantly higher IDH2 and succinate levels were found. Correlation analyses of mitochondrial functionality biomarkers with other blood markers revealed a significant relationship between CRP and ATP levels, with higher CRP significantly linked to lower ATP and a similar trend for succinate levels. Using the disease activity scale, we show that biomarkers such as IDH2, α-ketoglutarate, and succinate levels are significantly lower in patients with higher disease activity. Conclusion: We conclude that reduced metabolites and respiratory complexes associated with the TCA indicate mitochondrial bioenergetic failure in IBD patients. Besides, Krebs cycle metabolites can be a good marker of predisposition to the disease and the course of IBD. They can be easily determined in a blood sample taken from the patient. Pharmacological protection of mitochondria in individuals predisposed to IBD development and compensation for the changed function of mitochondria in persons with the developed disease may become a new approach to personalized therapies focused on restoring the proper activity of mitochondrial enzymes.
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