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: 4 complete abstracts (593 words), 10 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
Absorptive cells in the lining of the intestinal mucosa. They are differentiated epithelial cells with apical microvilli facing the intestinal lumen. Enterocytes are more abundant in the small intestine than in the large intestine. Their microvilli greatly increase the luminal surface area of the cell by 14- to 40 fold.
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: Enterocyte.
Where it fits in the MeSH classification
- Broader topics
- Intestinal Mucosa; Epithelial Cells
Related concepts
- Intestinal Mucosa
- Epithelial Cells
- Microvilli
- Small Intestine
- Large Intestine
Research landscape
PubMed indexes 3,655 records tagged with the MeSH heading “Enterocytes” (counts retrieved 2026-10-31). 636 of them (17.4%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 1,650 records.
Reviews account for 339 records (9.3%) and meta-analyses for 2. Randomized controlled trials number 28 (0.8%) 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 | 0 |
| 2000-2009 | 1,373 |
| 2010-2019 | 1,650 |
| 2020 onward | 636 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 339 | 9.3% |
| Meta-analyses | 2 | 0.1% |
| Randomized controlled trials | 28 | 0.8% |
Method: PubMed query "Enterocytes"[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 |
|---|---|---|---|---|
| SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues | 2020 | Research article Design not recorded in structured metadata | 1,980 | cc by PMID 32413319 · DOI · PMC7252096 |
| SARS-CoV-2 productively infects human gut enterocytes | 2020 | Research article Design not recorded in structured metadata | 1,384 | cc by PMID 32358202 · DOI · PMC7199907 |
| TMPRSS2 and TMPRSS4 promote SARS-CoV-2 infection of human small intestinal enterocytes | 2020 | Research article Design not recorded in structured metadata | 862 | cc by PMID 32404436 · DOI · PMC7285829 |
| Mathematical modeling reveals ferritin as the strongest cellular driver of dietary iron transfer block in enterocytes | 2025 | Research article Design not recorded in structured metadata | 2 | cc by PMID 40053535 · DOI · PMC11918390 |
SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues [1]
Abstract reading summary — source excerpts
- Opening excerpt
- There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19.
- Closing excerpt
- Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection.
- 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)
There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32413319 · DOI · PMC7252096
SARS-CoV-2 productively infects human gut enterocytes [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause coronavirus disease 2019 (COVID-19), an influenza-like disease that is primarily thought to infect the lungs with transmission through the respiratory route.
- Closing excerpt
- Therefore, the intestinal epithelium supports SARS-CoV-2 replication, and hSIOs serve as an experimental model for coronavirus infection and biology.
- 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 (117 words)
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause coronavirus disease 2019 (COVID-19), an influenza-like disease that is primarily thought to infect the lungs with transmission through the respiratory route. However, clinical evidence suggests that the intestine may present another viral target organ. Indeed, the SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2) is highly expressed on differentiated enterocytes. In human small intestinal organoids (hSIOs), enterocytes were readily infected by SARS-CoV and SARS-CoV-2, as demonstrated by confocal and electron microscopy. Enterocytes produced infectious viral particles, whereas messenger RNA expression analysis of hSIOs revealed induction of a generic viral response program. Therefore, the intestinal epithelium supports SARS-CoV-2 replication, and hSIOs serve as an experimental model for coronavirus infection and biology.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32358202 · DOI · PMC7199907
TMPRSS2 and TMPRSS4 promote SARS-CoV-2 infection of human small intestinal enterocytes [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Gastrointestinal symptoms and fecal shedding of SARS-CoV-2 RNA are frequently observed in COVID-19 patients.
- Closing excerpt
- Our results highlight the intestine as a potential site of SARS-CoV-2 replication, which may contribute to local and systemic illness and overall disease progression.
- 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 (122 words)
Gastrointestinal symptoms and fecal shedding of SARS-CoV-2 RNA are frequently observed in COVID-19 patients. However, it is unclear whether SARS-CoV-2 replicates in the human intestine and contributes to possible fecal-oral transmission. Here, we report productive infection of SARS-CoV-2 in ACE2+ mature enterocytes in human small intestinal enteroids. Expression of two mucosa-specific serine proteases, TMPRSS2 and TMPRSS4, facilitated SARS-CoV-2 spike fusogenic activity and promoted virus entry into host cells. We also demonstrate that viruses released into the intestinal lumen were inactivated by simulated human colonic fluid, and infectious virus was not recovered from the stool specimens of COVID-19 patients. Our results highlight the intestine as a potential site of SARS-CoV-2 replication, which may contribute to local and systemic illness and overall disease progression.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32404436 · DOI · PMC7285829
Mathematical modeling reveals ferritin as the strongest cellular driver of dietary iron transfer block in enterocytes [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Intestinal mucosal block is the transient reduction in iron absorption ability of intestinal epithelial cells (enterocytes) in response to previous iron exposures that occur at the cell scale.
- Closing excerpt
- Lastly, DMT1 endocytosis is shown to play a role in limiting total iron uptake by enterocytes but does not contribute to the decrease in total iron transfer across their basal membrane seen in the mucosal block.
- 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 (196 words)
Intestinal mucosal block is the transient reduction in iron absorption ability of intestinal epithelial cells (enterocytes) in response to previous iron exposures that occur at the cell scale. The block characteristics have been shown to depend both on iron exposure magnitude and temporality, and understanding block control will enable deeper understanding of how intestinal iron absorption contributes to pathological iron states. Three biochemical mechanisms implicated in driving the block behavior are divalent metal transporter 1 endocytosis, ferritin iron sequestration, and iron regulatory protein regulation of iron related protein expression. In this work, a model of enterocyte iron metabolism is built based on published experimental data that is capable of reproducing the mucosal block phenomena. The model is then used to estimate the quantitative contribution of each of the three mechanisms on the properties of the mucosal block. Analysis reveals that ferritin and iron regulatory proteins are the main intracellular mechanisms contributing to the mucosal block, findings congruent with experimental predictions. Lastly, DMT1 endocytosis is shown to play a role in limiting total iron uptake by enterocytes but does not contribute to the decrease in total iron transfer across their basal membrane seen in the mucosal block.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40053535 · DOI · PMC11918390
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 The mucus and mucins of the goblet cells and enterocytes provide the first defense line of the gastrointestinal tract and interact with the immune system [5]
- Research article Active sugar transport in health and disease [6]
- Research article Key discoveries in bile acid chemistry and biology and their clinical applications: history of the last eight decades [7]
- Research article Metabolism and functions of L-glutamate in the epithelial cells of the small and large intestines [8]
- Research article Shaping the intestinal brush border [9]
- Research article Absorption of vitamin A and carotenoids by the enterocyte: focus on transport proteins [10]
References
- Ziegler CGK, Allon SJ, Nyquist SK, Mbano IM, Miao VN, Tzouanas CN, et al.. SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues. . 2020. PMID 32413319 · DOI · PMC7252096
- Lamers MM, Beumer J, van der Vaart J, Knoops K, Puschhof J, Breugem TI, et al.. SARS-CoV-2 productively infects human gut enterocytes. . 2020. PMID 32358202 · DOI · PMC7199907
- Zang R, Gomez Castro MF, McCune BT, Zeng Q, Rothlauf PW, Sonnek NM, et al.. TMPRSS2 and TMPRSS4 promote SARS-CoV-2 infection of human small intestinal enterocytes. . 2020. PMID 32404436 · DOI · PMC7285829
- Masison J, Mendes P. Mathematical modeling reveals ferritin as the strongest cellular driver of dietary iron transfer block in enterocytes. . 2025. PMID 40053535 · DOI · PMC11918390
- Pelaseyed T, Bergström JH, Gustafsson JK, Ermund A, Birchenough GM, Schütte A, et al.. The mucus and mucins of the goblet cells and enterocytes provide the first defense line of the gastrointestinal tract and interact with the immune system. Immunol Rev. 2014. PMID 24942678 · DOI · PMC4281373
- Wright EM, Hirayama BA, Loo DF. Active sugar transport in health and disease. J Intern Med. 2007. PMID 17222166 · DOI
- Hofmann AF, Hagey LR. Key discoveries in bile acid chemistry and biology and their clinical applications: history of the last eight decades. J Lipid Res. 2014. PMID 24838141 · DOI · PMC4109754
- Blachier F, Boutry C, Bos C, Tomé D. Metabolism and functions of L-glutamate in the epithelial cells of the small and large intestines. Am J Clin Nutr. 2009. PMID 19571215 · DOI
- Crawley SW, Mooseker MS, Tyska MJ. Shaping the intestinal brush border. J Cell Biol. 2014. PMID 25422372 · DOI · PMC4242837
- Reboul E. Absorption of vitamin A and carotenoids by the enterocyte: focus on transport proteins. Nutrients. 2013. PMID 24036530 · DOI · PMC3798921
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.
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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.