ArticleCell death & disease2025
CKMT1 deficiency contributes to mitochondrial dysfunction and promotes intestinal epithelial cell apoptosis via reverse electron transfer-derived ROS in colitis.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Microbial metabolite Enterobactin impairs mitochondrial respiration and alleviates colitis.Gut microbes · 2026Article
- Programmed cell death in adenomyosis: mechanisms and future perspectives.Molecular biology reports · 2026Review
- Mitochondrial Dysfunction in Ulcerative Colitis: Pathogenic Mechanisms and Novel Therapeutics.Journal of biochemical and molecular toxicology · 2026Review
- Natural longevity modulator: aging modulatory effects of Eurycoma longifolia Jack polysaccharides in C. elegans and D. melanogaster.Biogerontology · 2026Article
- COX5A induces M2 macrophage polarization in chronic rhinosinusitis with nasal polyps through ROS generation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- WWP2 underlies ROS-induced granulosa cell apoptosis by promoting ubiquitination of BAK in polycystic ovary syndrome.Cell death & disease · 2026Article
- Dysfunction of mitochondria in intestinal epithelial cells: a key player in the pathogenesis of inflammatory bowel diseases.Gastroenterology report · 2026Review
- Lipopolysaccharide Upregulates Neuroinflammation, Oxidative Stress Responses, and Peroxiredoxins in Depression Models.Brain and behavior · 2026Article
- Machine learning-driven identification and experimental validation of key biomarkers in the bile acid metabolic pathway associated with ulcerative colitis.Frontiers in immunology · 2026Article
- Platelet CKB as a potential contributor to serum creatine kinase abnormalities and metastasis in cancer patients.Clinical and experimental medicine · 2025Article
- Gene editing in "cell villages" enables exploring disease-relevant mutations in many genetic backgrounds.bioRxiv : the preprint server for biology · 2025Article
- Crosstalk between mitochondrial dysfunction and benign prostatic hyperplasia: unraveling the intrinsic mechanisms.The Canadian journal of urology · 2025Review
- Mechanisms and therapeutic strategies of macrophages and neutrophils inducing ulcerative colitis progression.Frontiers in immunology · 2025Review
- Identification of Key Biomarkers and Immune Microenvironment Features in Ulcerative Colitis: An Integrated Analysis Using WGCNA and Multiple Machine Learning Algorithms.Journal of inflammation research · 2025Article
- The role and intrinsic connection of cellular senescence and cell death in inflammatory bowel disease.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction contributes to the pathogenesis of ulcerative colitis (UC). As a mitochondrial isozyme of creatine kinases, which control energy metabolism, CKMT1 is thought to be a critical molecule in biological processes. However, the specific role of CKMT1 in intestinal inflammation remains largely unknown. Here, we observed markedly decreased CKMT1 expression in the colon tissues of UC patients and dextran sodium sulfate (DSS)-induced colitis mice. We generated intestinal epithelial-specific CKMT1 knockout mice and demonstrated the key role of CKMT1 in mitochondrial homeostasis, intestinal epithelial barrier function, oxidative stress, and apoptosis. In the in vitro experiments, CKMT1 expression limited the activation of the intrinsic and extrinsic apoptotic pathways in IECs. Mechanistically, the loss of CKMT1 expression in IECs increased TNF-α-induced mitochondrial reactive oxygen species (ROS) generation via reverse electron transfer (RET). RET-ROS promoted mitochondrial permeability transition pore (mPTP) opening, ultimately resulting in cell apoptosis during intestinal inflammation. In conclusion, our data demonstrated that CKMT1 is important in maintaining intestinal homeostasis and mitochondrial function. This study provides a promising basis for future research and a potential therapeutic target for inflammatory bowel disease (IBD).
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