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NOD-Like Receptors in Intestinal Homeostasis and Epithelial Tissue Repair
Open accessAbstract
The intestinal epithelium constitutes a dynamic physical barrier segregating the luminal content from the underlying mucosal tissue. Following injury, the epithelial integrity is restored by rapid migration of intestinal epithelial cells (IECs) across the denuded area in a process known as wound healing. Hence, through a sequence of events involving restitution, proliferation and differentiation of IECs the gap is resealed and homeostasis reestablished. Relapsing damage followed by healing of the inflamed mucosa is a hallmark of several intestinal disorders including inflammatory bowel diseases (IBD). While several regulatory peptides, growth factors and cytokines stimulate restitution of the epithelial layer after injury, recent evidence in the field underscores the contribution of innate immunity in controlling this process. In particular, nucleotide-binding and oligomerization domain-like receptors (NLRs) play critical roles in sensing the commensal microbiota, maintaining homeostasis, and regulating intestinal inflammation. Here, we review the process of intestinal epithelial tissue repair and we specifically focus on the impact of NLR-mediated signaling mechanisms involved in governing epithelial wound healing during disease.
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“NLRs proteins are also responsible for maintaining gut barrier integrity by sensing the presence of commensal microbiota and the regulation of intestinal inflammation.172,173”
From Regulation of Intestinal Barrier Function by Microbial Metabolites (2021) · cites this paper as [172]
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Metadata
- Authors
- Parlato, M., & Yeretssian, G.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Tisch Cancer Institute (US)
- Corresponding author
- Yeretssian, Garabet
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2014-05-30
- Volume
- 15
- Issue
- 6
- Pages
- 9594-9627
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC4100112
- OpenAlex
- W2061048240
- Cited by
- 79
- References
- 297
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 4 · 2023: 7 · 2022: 6 · 2021: 8 · 2020: 4 · 2019: 8 · 2018: 13 · 2017: 6 · 2016: 7 · 2015: 5 · 2014: 2
- FWCI
- 0.88
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Leona M. and Harry B. Helmsley Charitable Trust
- Topics
- Health Sciences › Medicine › Gastroenterology › Inflammatory Bowel Disease
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- NOD-like receptors, intestinal epithelium, intestinal homeostasis, epithelial repair, tissue repair, intestinal inflammation, inflammatory bowel disease, innate immunity, commensal microbiota, epithelial restitution, intestinal epithelial cells
- MeSH terms
- Animals, Homeostasis, Humans, Immunity, Innate, Intestinal Mucosa, Wound Healing, Inflammatory Bowel Diseases, Toll-Like Receptors, Nod Signaling Adaptor Proteins, Inflammasomes
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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