ArticleNature communications2023
IFNγ-Stat1 axis drives aging-associated loss of intestinal tissue homeostasis and regeneration.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 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.
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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.
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Who cites it
35 citing papers in PubMed, 44 citations in OpenAlex.
- Intestinal Epithelial MHC-II at the Interface of Microbiota, Immunity, and Inflammation.International journal of molecular sciences · 2026Review
- Tissue and cellular spatiotemporal dynamics in colon aging.Nature biotechnology · 2026Article
- TNFR1 signaling connects inflammation to impaired fatty acid oxidation to drive intestinal stem cell aging.Nature aging · 2026Article
- Single-nucleus interrogation of primate small intestinal aging reveals NCoR1 decline as a conserved feature that is reversed by metformin.Nature aging · 2026Article
- Intestinal T cells in aging: implications for gut barrier integrity and inflammaging.GeroScience · 2026Review
- Maladaptive Inflammatory Signaling in Old Mice Impairs Colonic Regeneration by Promoting a Sustained Fetal-Like Epithelial State.Aging cell · 2026Article
- Lytic IFNγ is stored in cytotoxic granules and coreleased with granzyme B to mediate cytotoxic T lymphocyte killing.Cellular & molecular immunology · 2026Article
- Targeting NAT10 alleviates colonic senescence and elderly-onset colitis by disrupting N4-acetylation of DYRK1A.Nature communications · 2026Article
- Histone 3 lysine 36 trimethylation by SETD2 shapes an epigenetic landscape in intestinal stem cells to orchestrate lipid metabolism and attenuate cell senescence.Cell death & disease · 2026Article
- Rise or fall? Reconciling contested directions in human gut hormone aging.Frontiers in endocrinology · 2026Review
- Type I Interferons Drive the Gastrointestinal Inflammatory Response in a Mouse Model of Parkinson's Disease.Gastro hep advances · 2026Article
- Anti-uPAR CAR T cells reverse and prevent aging-associated defects in intestinal regeneration and fitness.Nature aging · 2026Article
- Organoid: a promising solution to current challenges in cancer immunotherapy.npj biomedical innovations · 2025Review
- Polyamines sustain epithelial regeneration in aged intestines by modulating protein homeostasis.Nature cell biology · 2025Article
- How stem cells respond to infection, inflammation and ageing.Nature reviews. Immunology · 2025Review
- Aging-related peroxisomal dysregulation disrupts intestinal stem cell differentiation through alterations of very long-chain fatty acid oxidation.PLoS biology · 2025Article
- Iron homeostasis and cell clonality drive cancer-associated intestinal DNA methylation drift in aging.Nature aging · 2025Article
- Immunosenescence and organoids: pathophysiology and therapeutic opportunities.Immunity & ageing : I & A · 2025Review
- IFN-γ is a direct driver of crypt hyperplasia in celiac disease.The Journal of clinical investigation · 2025Article
- Enteroendocrine cell differentiation: Implications for human disease.Molecular and cellular endocrinology · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
17 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The influence of aging on intestinal stem cells and their niche can explain underlying causes for perturbation in their function observed during aging. Molecular mechanisms for such a decrease in the functionality of intestinal stem cells during aging remain largely undetermined. Using transcriptome-wide approaches, our study demonstrates that aging intestinal stem cells strongly upregulate antigen presenting pathway genes and over-express secretory lineage marker genes resulting in lineage skewed differentiation into the secretory lineage and strong upregulation of MHC class II antigens in the aged intestinal epithelium. Mechanistically, we identified an increase in proinflammatory cells in the lamina propria as the main source of elevated interferon gamma (IFNγ) in the aged intestine, that leads to the induction of Stat1 activity in intestinal stem cells thus priming the aberrant differentiation and elevated antigen presentation in epithelial cells. Of note, systemic inhibition of IFNγ-signaling completely reverses these aging phenotypes and reinstalls regenerative capacity of the aged intestinal epithelium.
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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.