ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2013
Irgm1-deficient mice exhibit Paneth cell abnormalities and increased susceptibility to acute intestinal inflammation.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
107 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.
- Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Iron and Other Metal Ions in Human Health and Disease.MedComm · 2026Review
- Identification of key mitochondria-related genes in necrotizing enterocolitis using single-cell hdWGCNA and experimental verification.Pediatric research · 2026Article
- Cytokine networks in Paneth cell regulation.Mucosal immunology · 2026Review
- IRGM1-IRF7 Axis Controls Macrophage Chemotaxis to Orchestrate Skeletal Muscle Regeneration.Inflammation · 2026Article
- Paneth cells as orchestrators of epithelial barrier defense and emerging therapeutic targets in inflammatory bowel disease.Seminars in immunopathology · 2026Review
- The importance of mitochondria and mitochondrial calcium signaling in health and disease: an updated outlook on inflammation.Journal of translational medicine · 2026Review
- Mitophagy in inflammatory bowel disease: regulatory mechanisms and therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- Mitophagy-related molecular signatures in ulcerative colitis revealed by machine learning and molecular dynamics.Frontiers in genetics · 2026Article
- Mitophagy in the pathogenesis and management of disease.Cell research · 2026Review
- Differential roles for Irgm1 in myeloid cells for immune resistance to pathogenic bacteria.Journal of leukocyte biology · 2025Article
- From Cytokines to Biomarkers: Mapping the Immunopathology of Inflammatory Bowel Disease.Cells · 2025Review
- Article
- The clinical application value of the biomarkers based on autophagy screening in the diagnosis and monitoring of inflammatory bowel disease in pediatric patients.European journal of pediatrics · 2025Article
- Gut microbiota modulate intestinal inflammation by endoplasmic reticulum stress-autophagy-cell death signaling axis.Journal of animal science and biotechnology · 2025Review
- BECLIN-1/BECN1 at the barrier: a gatekeeper of epithelial and endothelial homeostasis.Autophagy reports · 2025Review
- Autophagy and Bacterial infections.Autophagy reports · 2025Review
- Autophagy in inflammatory bowel disease: immunization, etiology, and therapeutic potential.Frontiers in immunology · 2025Review
- Type I interferon signaling and peroxisomal dysfunction contribute to enhanced inflammatory cytokine production in IRGM1-deficient macrophages.The Journal of biological chemistry · 2024Article
- Autophagy in Disease Onset and Progression.Aging and disease · 2024Review
47 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
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Crohn's disease (CD) is a chronic, immune-mediated, inflammatory disorder of the intestine that has been linked to numerous susceptibility genes, including the immunity-related GTPase (IRG) M (IRGM). IRGs comprise a family of proteins known to confer resistance to intracellular infections through various mechanisms, including regulation of phagosome processing, cell motility, and autophagy. However, despite its association with CD, the role of IRGM and other IRGs in regulating intestinal inflammation is unclear. We investigated the involvement of Irgm1, an ortholog of IRGM, in the genesis of murine intestinal inflammation. After dextran sodium sulfate exposure, Irgm1-deficient [Irgm1 knockout (KO)] mice showed increased acute inflammation in the colon and ileum, with worsened clinical responses. Marked alterations of Paneth cell location and granule morphology were present in Irgm1 KO mice, even without dextran sodium sulfate exposure, and were associated with impaired mitophagy and autophagy in Irgm1 KO intestinal cells (including Paneth cells). This was manifested by frequent tubular and swollen mitochondria and increased LC3-positive autophagic structures. Interestingly, these LC3-positive structures often contained Paneth cell granules. These results suggest that Irgm1 modulates acute inflammatory responses in the mouse intestine, putatively through the regulation of gut autophagic processes, that may be pivotal for proper Paneth cell functioning.
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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.