Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (528 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Lining of the intestines, consisting of an inner epithelium, a middle lamina propria, and an outer muscularis mucosae. In the small intestine, the mucosa is characterized by a series of folds and abundance of absorptive cells (enterocytes) with microvilli.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Mucosa, Intestinal; Intestinal Epithelium; Epithelium, Intestinal; Intestinal Glands; Gland, Intestinal; Glands, Intestinal; Intestinal Gland.
Where it fits in the MeSH classification
- Broader topics
- Intestines; Mucous Membrane
- Narrower topics
- Enterocytes; Goblet Cells; Paneth Cells
- See also
- Intestinal Secretions
Related concepts
- Intestines
- Epithelium
- Mucous Membrane
- Mucous Membrane
- Small Intestine
- Enterocytes
- Microvilli
Research landscape
PubMed indexes 107,164 records tagged with the MeSH heading “Intestinal Mucosa” (counts retrieved 2026-10-31). 15,361 of them (14.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 41,617 records.
Reviews account for 11,862 records (11.1%) and meta-analyses for 172. Randomized controlled trials number 1,390 (1.3%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 41,617 |
| 2000-2009 | 22,093 |
| 2010-2019 | 28,093 |
| 2020 onward | 15,361 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 11,862 | 11.1% |
| Meta-analyses | 172 | 0.2% |
| Randomized controlled trials | 1,390 | 1.3% |
Method: PubMed query "Intestinal Mucosa"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| CD163 and Tim-4 identify resident intestinal macrophages that are spatially regulated by TGF-β | 2026 | Research article Design not recorded in structured metadata | 12 | cc by PMID 42012484 · DOI · PMC13098488 |
| Metformin inhibits mitochondrial complex I in intestinal epithelium to promote glycaemic control | 2026 | Research article Design not recorded in structured metadata | 11 | cc by PMID 42103929 · DOI · PMC13303093 |
| Intestinal Stem Cells From Patients With Inflammatory Bowel Disease Retain an Epigenetic Memory of Inflammation | 2026 | Research article Design not recorded in structured metadata | 10 | cc by PMID 41903684 · DOI · PMC13196144 |
CD163 and Tim-4 identify resident intestinal macrophages that are spatially regulated by TGF-β [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Macrophages localize in sub-tissular niches associated with their ontogeny and activity.
- Closing excerpt
- Employing transgenic mice, we demonstrate a critical role for TGF-β signalling in maintaining the identity of long-lived LP but not S/M macrophages and that macrophage-derived TGF-β1 is required to instruct intestinal macrophage identity after development.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (159 words)
Macrophages localize in sub-tissular niches associated with their ontogeny and activity. In the intestine, a paradigm has emerged that long-lived macrophages are present in the muscular layer, while highly monocyte-replenished populations are found in the lamina propria (LP). Whether long-lived macrophages are restricted in such a simplified manner has not been well explored. Moreover, the impact of specific gut-associated factors on macrophage identity across intestinal tissue layers is unknown. We generated scRNA-seq data from WT and Ccr2-/- mice to identify phenotypic features of long-lived macrophage populations in distinct intestinal layers and identified CD163 as a marker to distinguish submucosal/muscularis (S/M) from LP macrophages. Challenging the emerging paradigm, long-lived macrophages were found in the LP and S/M, with distinct transcriptomes and responsiveness to proinflammatory stimuli. Employing transgenic mice, we demonstrate a critical role for TGF-β signalling in maintaining the identity of long-lived LP but not S/M macrophages and that macrophage-derived TGF-β1 is required to instruct intestinal macrophage identity after development.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42012484 · DOI · PMC13098488
Metformin inhibits mitochondrial complex I in intestinal epithelium to promote glycaemic control [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Metformin is a versatile biguanide drug primarily prescribed for type II diabetes.
- Closing excerpt
- Notably, the efficacy of phenformin, another biguanide, and berberine, a structurally unrelated nutraceutical, similarly depends on intestine-specific mitochondrial complex I inhibition, underscoring a shared therapeutic mechanism.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (158 words)
Metformin is a versatile biguanide drug primarily prescribed for type II diabetes. Despite its extensive use, the mechanisms underlying its clinical effects, including attenuated postprandial glucose excursions and elevated intestinal glucose uptake, remain unclear. Here we map these and other effects of metformin to intestine-specific mitochondrial complex I inhibition. Using human metabolomic data and an orthogonal genetics approach in male mice, we demonstrate that metformin suppresses citrulline synthesis, a metabolite generated exclusively by small intestine mitochondria, and increases GDF15 by inhibiting the mitochondrial respiratory chain at complex I. This inhibition co-opts the intestines to function as a glucose sink, driving the uptake of excess glucose and its conversion to lactate and lactoyl-phenylalanine. We also find that glucose lowering by metformin is due to repeated bolus exposure rather than a cumulative chronic response. Notably, the efficacy of phenformin, another biguanide, and berberine, a structurally unrelated nutraceutical, similarly depends on intestine-specific mitochondrial complex I inhibition, underscoring a shared therapeutic mechanism.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42103929 · DOI · PMC13303093
Intestinal Stem Cells From Patients With Inflammatory Bowel Disease Retain an Epigenetic Memory of Inflammation [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Background & aimsIntestinal epithelial damage and impaired repair are hallmarks of ulcerative colitis (UC), even after inflammation resolves.
- Closing excerpt
- Although this may support epithelial adaptation to secondary insults, it may predispose tissue to relapse in patients with UC.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (211 words)
Background & aimsIntestinal epithelial damage and impaired repair are hallmarks of ulcerative colitis (UC), even after inflammation resolves. Intestinal stem cells (ISCs) can retain stable epigenetic changes after inflammation, highlighting the potential for long-lived epithelial memory in the gut. Inflammatory injury in barrier tissues induces epigenetic memory in epithelial stem cells, and the tendency of UC to relapse at previously inflamed sites led us to hypothesize that ISCs from patients with inflammatory bowel disease acquire lasting memory of prior inflammation.MethodsTo test this, we derived colonic organoids from inflamed (I) and noninflamed regions of the same patients with UC and propagated in long-term culture.ResultsChromatin profiling revealed 2252 accessible regions unique to I organoids, associated with stress response, repair, and inflammatory genes. Although these regions remained accessible, ∼95% of associated genes were not upregulated in I organoids, indicating a primed state. Upon inflammatory or injury re-challenge, I organoids exhibited heightened transcriptional responses and accelerated wound closure, despite reduced clonogenicity and impaired barrier function, indicating a retained inflammatory memory program.ConclusionsOur findings demonstrate that human ISCs retain a chromatin-based memory of inflammation that persists in the absence of immune cues and shapes future responses to injury. Although this may support epithelial adaptation to secondary insults, it may predispose tissue to relapse in patients with UC.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41903684 · DOI · PMC13196144
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Systematic review with meta-analysis: mucosal healing is associated with improved long-term outcomes in Crohn's disease [4]
- Research article The intestinal barrier: a pivotal role in health, inflammation, and cancer [5]
- Research article Intestinal mucus and their glycans: A habitat for thriving microbiota [6]
- Research article Systematic review and meta-analysis of histopathological factors influencing the risk of lymph node metastasis in early colorectal cancer [7]
- Research article Meta-analysis of the turnover of intestinal epithelia in preclinical animal species and humans [8]
- Research article The gut-liver axis in sepsis: interaction mechanisms and therapeutic potential [9]
References
- Jayaraman V, Prise IE, Kästele V, Tamburrano S, Wemyss K, Bridgeman HM, et al.. CD163 and Tim-4 identify resident intestinal macrophages that are spatially regulated by TGF-β. . 2026. PMID 42012484 · DOI · PMC13098488
- Sebo ZL, Chakrabarty RP, Grant RA, D'Alessandro KB, Koss AR, Blum JLE, et al.. Metformin inhibits mitochondrial complex I in intestinal epithelium to promote glycaemic control. . 2026. PMID 42103929 · DOI · PMC13303093
- Hamdan FH, Farhadipour M, Perez I, Kossick K, Smith H, Edwinson A, et al.. Intestinal Stem Cells From Patients With Inflammatory Bowel Disease Retain an Epigenetic Memory of Inflammation. . 2026. PMID 41903684 · DOI · PMC13196144
- Shah SC, Colombel JF, Sands BE, Narula N. Systematic review with meta-analysis: mucosal healing is associated with improved long-term outcomes in Crohn's disease. Aliment Pharmacol Ther. 2016. PMID 26607562 · DOI
- Neurath MF, Artis D, Becker C. The intestinal barrier: a pivotal role in health, inflammation, and cancer. Lancet Gastroenterol Hepatol. 2025. PMID 40086468 · DOI
- Luis AS, Hansson GC. Intestinal mucus and their glycans: A habitat for thriving microbiota. Cell Host Microbe. 2023. PMID 37442097 · DOI · PMC10348403
- Beaton C, Twine CP, Williams GL, Radcliffe AG. Systematic review and meta-analysis of histopathological factors influencing the risk of lymph node metastasis in early colorectal cancer. Colorectal Dis. 2013. PMID 23331927 · DOI
- Darwich AS, Aslam U, Ashcroft DM, Rostami-Hodjegan A. Meta-analysis of the turnover of intestinal epithelia in preclinical animal species and humans. Drug Metab Dispos. 2014. PMID 25233858 · DOI
- Zhang X, Liu H, Hashimoto K, Yuan S, Zhang J. The gut-liver axis in sepsis: interaction mechanisms and therapeutic potential. Crit Care. 2022. PMID 35831877 · DOI · PMC9277879
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.