ReviewNature reviews. Gastroenterology & hepatology2018
Mitochondrial function - gatekeeper of intestinal epithelial cell homeostasis.
Review in Nature reviews. Gastroenterology & hepatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers.
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
159 citing papers in PubMed, 302 citations in OpenAlex.
- Trial
- IL-10-STAT3 axis preserves epithelial mitochondrial homeostasis during bacterial challenge.Gut microbes · 2026Article
- Mapping mitochondria-associated research in inflammatory bowel disease: A bibliometric and network analysis.Medicine · 2026Article
- Effects of cuproptosis and its application in inflammatory bowel disease (Review).International journal of molecular medicine · 2026Review
- Multi-level aggregation analysis of microbiome composition and host gene expression reveals associations with systemic and local immunity.Microbiology spectrum · 2026Article
- Selenium Nanoparticles Alleviate Intestinal Epithelial Barrier Dysfunction by Coordinating Mitochondria-lysosome Communication under Dual Organelle Stress.Biological trace element research · 2026Article
- Shenling Baizhu powder reduced the oxidative stress and mitochondrial damage during ulcerative colitisthe Kelch-like ECH-associated protein 1-NF-E2-related factor 2/nuclear factor kappa B pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- Colonic epithelial regeneration shapes susceptibility tobioRxiv : the preprint server for biology · 2026Article
- The lipid transfer protein STARD7 controls intestinal tumor development in a context-dependent manner.EMBO molecular medicine · 2026Article
- Dietary supplementation with putrescine improves meat quality, enhances intestinal development, and modulates the intestinal microbiota in Wenchang chickens.Poultry science · 2026Article
- Vibrio proteolyticus DCF12.2 postbiotic modulates intestinal metabolic and immune pathways in zebrafish.Applied microbiology and biotechnology · 2026Article
- Roles and related underlying mechanisms of mitochondrial RNA modification in cancer progression.Acta pharmacologica Sinica · 2026Review
- O-GlcNAcylation regulates PPAR-driven metabolic programming in intestinal stem cells.bioRxiv : the preprint server for biology · 2026Article
- Butyrate extends health and lifespan in mice with mitochondrial deficiency.Nature communications · 2026Article
- An organoid-based evaluation of Bacillus amyloliquefaciens SC06 in alleviating oxidative damage via Wnt signaling.BMC veterinary research · 2026Article
- Selective autophagic degradation of glycolytic activator PFKFB3 contributes to maintaining intestinal epithelial barrier in inflammatory bowel disease.International journal of molecular medicine · 2026Article
- Microvillus inclusion disease-associated MYO5B deficiency impairs endosome-to-mitochondrion iron transfer.Gastroenterology report · 2026Article
- Danthron Attenuates Intestinal Inflammation by Modulating Oxidative Stress via the EGFR-PI3K-AKT and Nrf2-HO-1 Pathways.Antioxidants (Basel, Switzerland) · 2026Article
- Butyrate extends health and lifespan in mice with mitochondrial deficiency.bioRxiv : the preprint server for biology · 2026Article
- Lactobacillus johnsonii JJB3 Ameliorates Oxidative Stress-Induced Intestinal Injury and Mitochondrial Damage by Promoting BNIP3L-Mediated Mitophagy.Probiotics and antimicrobial proteins · 2026Article
99 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intestinal epithelium is a multicellular interface in close proximity to a dense microbial milieu that is completely renewed every 3-5 days. Pluripotent stem cells reside at the crypt, giving rise to transient amplifying cells that go through continuous steps of proliferation, differentiation and finally anoikis (a form of programmed cell death) while migrating upwards to the villus tip. During these cellular transitions, intestinal epithelial cells (IECs) possess distinct metabolic identities reflected by changes in mitochondrial activity. Mitochondrial function emerges as a key player in cell fate decisions and in coordinating cellular metabolism, immunity, stress responses and apoptosis. Mediators of mitochondrial signalling include molecules such as ATP and reactive oxygen species and interrelate with pathways such as the mitochondrial unfolded protein response (MT-UPR) and AMP kinase signalling, in turn affecting cell cycle progression and stemness. Alterations in mitochondrial function and MT-UPR activation are integral aspects of pathologies, including IBD and cancer. Mitochondrial signalling and concomitant changes in metabolism contribute to intestinal homeostasis and regulate IEC dedifferentiation-differentiation programmes in the context of diseases, suggesting that mitochondrial function as a cellular checkpoint critically contributes to disease outcome. This Review highlights mitochondrial function and MT-UPR signalling in epithelial cell stemness, differentiation and lineage commitment and illustrates mitochondrial function in intestinal diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.