ArticleCellular and molecular gastroenterology and hepatology2020
Insulin-like Growth Factor-1 and mTORC1 Signaling Promote the Intestinal Regenerative Response After Irradiation Injury.
Article in Cellular and molecular gastroenterology and hepatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 38 citations in OpenAlex.
- Paneth cell-derived Notch ligands DLL1 and DLL4 are crucial for intestinal crypt base stem cells.bioRxiv : the preprint server for biology · 2026Article
- Biological Insights into Intestinal Adaptation from Preclinical Models of Short Bowel Syndrome.Cells · 2026Review
- A spatial and temporal transcriptomic atlas of mouse intestinal regeneration in the jejunum.Nature communications · 2026Article
- Radiomitigators: Breakthroughs in Post-Radiation Recovery.Antioxidants (Basel, Switzerland) · 2026Review
- Myosin VB is critical for progenitor cell identity and function in the intestine.Stem cell reports · 2026Article
- Paligenosis: dual potential of mature cell plasticity in regeneration and tumorigenesis.MedScience · 2026Review
- Gut microbiota-derived metabolites and IL-22 signaling in inflammatory bowel disease: context-dependent regulation of mucosal repair and inflammation.Frontiers in immunology · 2026Review
- Citral impairs intestinal changes caused by ulcerative colitis through modulation of antioxidant, anti-inflammatory and healing activities.Inflammopharmacology · 2026Article
- Tissue-adapted Tregs harness inflammatory signals to promote intestinal repair from therapy-related injury.Signal transduction and targeted therapy · 2025Article
- The Effects of FeedingMicroorganisms · 2025Article
- Targeting the Gut-Brain Axis Through Insulin-like Growth Factors: Therapeutic Implications and Future Directions.Journal of molecular neuroscience : MN · 2025Review
- The microbial metabolite desaminotyrosine protects against graft-versus-host disease via mTORC1 and STING-dependent intestinal regeneration.Nature communications · 2025Article
- Phosphatidylinositol 3-Kinase Signaling Enhances Intestinal Crypt Epithelial Cell Recovery after Radiation.The American journal of pathology · 2025Article
- Advanced Microbiome Therapeutics Accelerate MASLD Recovery by Restoring Intestinal Microbiota Equilibrium and the Gut-Liver Axis in a Mouse Model.Journal of agricultural and food chemistry · 2025Article
- Effects of Cholinergic and Opioid Antagonists on In Vitro Release of Met-Enkephalin, Somatostatin and Insulin-like Growth Factor-1 by and PENK Expression in Crop, Proventriculus and Duodenum of Newly Hatched Chickens.Animals : an open access journal from MDPI · 2025Article
- Systemic IGF-1 administration prevents traumatic brain injury induced gut permeability, dysmorphia, dysbiosis, and the increased number of immature dentate granule cells.Acta neuropathologica communications · 2025Article
- Impact of initial postweaning feed intake on weanling piglet metabolism, gut health, and immunity.Journal of animal science · 2025Article
- Mechanisms of Insulin Signaling as a Potential Therapeutic Method in Intestinal Diseases.Cells · 2024Review
- Activation of fetal-like molecular programs during regeneration in the intestine and beyond.Cell stem cell · 2024Review
- Genetic Upregulation of Activated Protein C Mitigates Delayed Effects of Acute Radiation Exposure in the Mouse Plasma.Metabolites · 2024Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsIntestinal crypts have a remarkable capacity to regenerate after injury from loss of crypt base columnar (CBC) stem cells. After injury, facultative stem cells (FSCs) are activated to replenish the epithelium and replace lost CBCs. Our aim was to assess the role of insulin-like growth factor-1 (IGF-1) to activate FSCs for crypt repair.
methodsThe intestinal regenerative response was measured after whole body 12-Gy γ-irradiation of adult mice. IGF-1 signaling or its downstream effector mammalian target of rapamycin complex 1 (mTORC1) was inhibited by administering BMS-754807 or rapamycin, respectively. Mice with inducible Rptor gene deletion were studied to test the role of mTORC1 signaling in the intestinal epithelium. FSC activation post-irradiation was measured by lineage tracing.
resultsWe observed a coordinate increase in growth factor expression, including IGF-1, at 2 days post-irradiation, followed by a surge in mTORC1 activity during the regenerative phase of crypt repair at day 4. IGF-1 was localized to pericryptal mesenchymal cells, and IGF-1 receptor was broadly expressed in crypt progenitor cells. Inhibition of IGF-1 signaling via BMS-754807 treatment impaired crypt regeneration after 12-Gy irradiation, with no effect on homeostasis. Similarly, rapamycin inhibition of mTORC1 during the growth factor surge blunted the regenerative response. Analysis of Villin-CreER
conclusionsOur study shows that IGF-1 signaling through mTORC1 drives crypt regeneration. We propose that IGF-1 release from pericryptal cells stimulates mTORC1 in FSCs to regenerate lost CBCs.
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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.