ArticleCell proliferation2022
The inhibition of enterocyte proliferation by lithocholic acid exacerbates necrotizing enterocolitis through downregulating the Wnt/β-catenin signalling pathway.
Article in Cell proliferation, 2022. 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, 21 citations in OpenAlex.
- Gut microbiota and aging: current understanding and future perspectives.Molecular biomedicine · 2026Review
- IFN-γ and TNF-α Impair Lung Development by Upregulating SMAD7 to Inhibit TGF-β Signaling Pathway and ECM Dysregulation.Inflammation · 2026Article
- Disruption of bile acid homeostasis potentiates Paneth cell ablation by activating the intestinal Farnesoid X receptor in necrotizing enterocolitis.NPJ biofilms and microbiomes · 2026Article
- Gut microbial metabolites in inflammation-associated colorectal cancer: mechanisms and therapeutic implications.Frontiers in microbiology · 2026Review
- The alteration of bile acids and gut microbiota is associated with intestinal barrier dysfunction and inflammaging in human.Frontiers in aging · 2026Article
- Impact of Diquat on the Intestinal Health and the Composition and Function of the Gut Microbiome.Antioxidants (Basel, Switzerland) · 2025Review
- Gut Microbiota-Derived Metabolites and Their Role in the Pathogenesis of Necrotizing Enterocolitis in Preterm Infants: A Narrative Review.Metabolites · 2024Review
- Hydroxytyrosol Alleviates Intestinal Oxidative Stress by Regulating Bile Acid Metabolism in a Piglet Model.International journal of molecular sciences · 2024Article
- The role of the gut microbiota in tumor, immunity, and immunotherapy.Frontiers in immunology · 2024Review
- Deoxycholic acid aggravates necrotizing enterocolitis through downregulation of mesenchymal-epithelial transition factor expression.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024Article
- Article
- Small molecule metabolites: discovery of biomarkers and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Necroptosis of macrophage is a key pathological feature in biliary atresia via GDCA/S1PR2/ZBP1/p-MLKL axis.Cell death & disease · 2023Article
- The inhibition of enterocyte proliferation by lithocholic acid exacerbates necrotizing enterocolitis through downregulating the Wnt/β-catenin signalling pathway.Cell proliferation · 2022Article
- Succinate aggravates intestinal injury in mice with necrotizing enterocolitis.Frontiers in cellular and infection microbiology · 2022Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesNecrotizing enterocolitis (NEC) is a catastrophic gastrointestinal emergency in preterm infants, whose exact aetiology remains unknown. The role of lithocholic acid (LCA), a key component of secondary bile acids (BAs), in NEC is unclear.
methodsClinical data were collected to analyse the changes of BAs in NEC patients. In vitro studies, the cell proliferation and cell death were assessed. In vivo experiments, the newborn rats were administered with low or high dose of LCA and further induced NEC.
resultsClinically, compared with control group, total BAs in the NEC patients were significantly higher when NEC occurred. In vitro, LCA treatment significantly inhibited the cell proliferation through arresting cell cycle at G1/S phase without inducing apoptosis or necroptosis. Mechanistically, the Wnt/β-catenin pathway was involved. In vivo, LCA inhibited intestinal cell proliferation leading to disruption of intestinal barrier, and thereby increased the severity of NEC. Specifically, LCA supplementation caused higher levels of FITC-labelled dextran in serum, reduced PCNA expression and inhibited the activity of Wnt/β-catenin pathway in enterocytes. The LC-MS/MS test found that LCA was significantly higher in intestinal tissue of NEC group, and more obviously in the NEC-L and NEC-H group compared with the DM group.
conclusionLCA exacerbates NEC by inhibiting intestinal cell proliferation through downregulating the Wnt/β-catenin pathway.
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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.