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 (651 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
A membrane of squamous epithelial cells, the mesothelial cells, covered by apical microvilli that allow rapid absorption of fluid and particles in the peritoneal cavity. The peritoneum is divided into parietal and visceral components. The parietal peritoneum covers the inside of the abdominal wall. The visceral peritoneum covers the intraperitoneal organs. The double-layered peritoneum forms the mesentery that suspends these organs from the abdominal wall.
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: Peritoneum, Parietal; Parietal Peritoneum; Peritoneum, Visceral; Visceral Peritoneum; Parametrium; Parametriums.
Where it fits in the MeSH classification
- Broader topics
- Abdominal Cavity; Serous Membrane
- Narrower topics
- Douglas' Pouch; Mesentery; Omentum; Peritoneal Cavity; Peritoneal Stomata
- See also
- Ascitic Fluid; Laparoscopy
Related concepts
- Epithelial Cells
- Microvilli
- Peritoneal Cavity
- Abdominal Wall
- Mesentery
Research landscape
PubMed indexes 46,188 records tagged with the MeSH heading “Peritoneum” (counts retrieved 2026-10-31). 3,800 of them (8.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 25,620 records.
Reviews account for 3,000 records (6.5%) and meta-analyses for 205. Randomized controlled trials number 503 (1.1%) 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 | 25,620 |
| 2000-2009 | 8,421 |
| 2010-2019 | 8,347 |
| 2020 onward | 3,800 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 3,000 | 6.5% |
| Meta-analyses | 205 | 0.4% |
| Randomized controlled trials | 503 | 1.1% |
Method: PubMed query "Peritoneum"[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 |
|---|---|---|---|---|
| Neutrophils direct preexisting matrix to initiate repair in damaged tissues | 2022 | Research article Design not recorded in structured metadata | 100 | cc by PMID 35354953 · DOI · PMC8986538 |
| Mechanisms of Peritoneal Fibrosis: Focus on Immune Cells-Peritoneal Stroma Interactions | 2021 | Systematic review Design not recorded in structured metadata | 87 | cc by PMID 33854496 · DOI · PMC8039516 |
| Genetic fate-mapping reveals surface accumulation but not deep organ invasion of pleural and peritoneal cavity macrophages following injury | 2021 | Research article Design not recorded in structured metadata | 47 | cc by PMID 34001904 · DOI · PMC8129080 |
| Compound design of a patient-derived 3D cell culture system modelling early peritoneal endometriosis | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41392657 · DOI · PMC12919959 |
Neutrophils direct preexisting matrix to initiate repair in damaged tissues [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Internal organs heal injuries with new connective tissue, but the cellular and molecular events of this process remain obscure.
- Closing excerpt
- Matrix transfer was thus an early event of wound repair and provides a therapeutic window to dampen scaring across a range of conditions.
- 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 (140 words)
Internal organs heal injuries with new connective tissue, but the cellular and molecular events of this process remain obscure. By tagging extracellular matrix around the mesothelium lining in mouse peritoneum, liver and cecum, here we show that preexisting matrix was transferred across organs into wounds in various injury models. Using proteomics, genetic lineage-tracing and selective injury in juxtaposed organs, we found that the tissue of origin for the transferred matrix likely dictated the scarring or regeneration of the healing tissue. Single-cell RNA sequencing and genetic and chemical screens indicated that the preexisting matrix was transferred by neutrophils dependent on the HSF-integrin AM/B2-kindlin3 cascade. Pharmacologic inhibition of this axis prevented matrix transfer and the formation of peritoneal adhesions. Matrix transfer was thus an early event of wound repair and provides a therapeutic window to dampen scaring across a range of conditions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35354953 · DOI · PMC8986538
Mechanisms of Peritoneal Fibrosis: Focus on Immune Cells-Peritoneal Stroma Interactions [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Peritoneal fibrosis is characterized by abnormal production of extracellular matrix proteins leading to progressive thickening of the submesothelial compact zone of the peritoneal membrane.
- Closing excerpt
- The understanding of cellular and molecular mechanisms underlying fibrosis of the peritoneal membrane has both a basic and a translational relevance, since it may be useful for setup of therapies aimed at counteracting the deterioration as well as restoring the homeostasis of the peritoneal membrane.
- 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 (210 words)
Peritoneal fibrosis is characterized by abnormal production of extracellular matrix proteins leading to progressive thickening of the submesothelial compact zone of the peritoneal membrane. This process may be caused by a number of insults including pathological conditions linked to clinical practice, such as peritoneal dialysis, abdominal surgery, hemoperitoneum, and infectious peritonitis. All these events may cause acute/chronic inflammation and injury to the peritoneal membrane, which undergoes progressive fibrosis, angiogenesis, and vasculopathy. Among the cellular processes implicated in these peritoneal alterations is the generation of myofibroblasts from mesothelial cells and other cellular sources that are central in the induction of fibrosis and in the subsequent functional deterioration of the peritoneal membrane. Myofibroblast generation and activity is actually integrated in a complex network of extracellular signals generated by the various cellular types, including leukocytes, stably residing or recirculating along the peritoneal membrane. Here, the main extracellular factors and the cellular players are described with emphasis on the cross-talk between immune system and cells of the peritoneal stroma. The understanding of cellular and molecular mechanisms underlying fibrosis of the peritoneal membrane has both a basic and a translational relevance, since it may be useful for setup of therapies aimed at counteracting the deterioration as well as restoring the homeostasis of the peritoneal membrane.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33854496 · DOI · PMC8039516
Genetic fate-mapping reveals surface accumulation but not deep organ invasion of pleural and peritoneal cavity macrophages following injury [3]
Abstract reading summary — source excerpts
- Opening excerpt
- During injury, monocytes are recruited from the circulation to inflamed tissues and differentiate locally into mature macrophages, with prior reports showing that cavity macrophages of the peritoneum and pericardium invade deeply into the respective organs to promote repair.
- Closing excerpt
- Our in vivo genetic targeting approach thus provides a reliable method to identify and characterize cavity macrophages during their development and in tissue repair and regeneration, and distinguishes these cells from other lineages.
- 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 (137 words)
During injury, monocytes are recruited from the circulation to inflamed tissues and differentiate locally into mature macrophages, with prior reports showing that cavity macrophages of the peritoneum and pericardium invade deeply into the respective organs to promote repair. Here we report a dual recombinase-mediated genetic system designed to trace cavity macrophages in vivo by intersectional detection of two characteristic markers. Lineage tracing with this method shows accumulation of cavity macrophages during lung and liver injury on the surface of visceral organs without penetration into the parenchyma. Additional data suggest that these peritoneal or pleural cavity macrophages do not contribute to tissue repair and regeneration. Our in vivo genetic targeting approach thus provides a reliable method to identify and characterize cavity macrophages during their development and in tissue repair and regeneration, and distinguishes these cells from other lineages.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34001904 · DOI · PMC8129080
Compound design of a patient-derived 3D cell culture system modelling early peritoneal endometriosis [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Peritoneal endometriosis causes pelvic pain and infertility, but the underlying mechanisms related to these symptoms are not fully understood.
- Closing excerpt
- Our modifiable superficial endometriosis model allows for further refinement to determine the underlying molecular mechanism(s) involved in endometriotic lesion formation.
- 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 (164 words)
Peritoneal endometriosis causes pelvic pain and infertility, but the underlying mechanisms related to these symptoms are not fully understood. Endometriosis diagnosis is typically delayed; thus, patient samples are unsuitable to study early endometriosis formation in situ. We generated a 3D co-culture model of early peritoneal endometriosis using patient-derived primary cells, providing unique opportunities to examine endometriotic lesion initiation and progression. The successful assembly of a simple peritoneum layer model comprising a mesothelial monolayer, basement membrane and underlying fibroblasts was achieved by embedding human peritoneal fibroblasts in a Matrigel-collagen I matrix and subsequent seeding with a layer of donor-matched human peritoneal mesothelial cells, while secretion of tissue plasminogen activator demonstrated functional mesothelial physiology. Endometrial epithelial organoids were co-cultured with endometrial stromal cells to form endometrial assembloids mimicking shed endometrial tissue fragments at menstruation, which adhered onto the peritoneal layer model, simulating early endometriotic lesion formation. Our modifiable superficial endometriosis model allows for further refinement to determine the underlying molecular mechanism(s) involved in endometriotic lesion formation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41392657 · DOI · PMC12919959
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 mesentery: structure, function, and role in disease [5]
- Research article Intraperitoneal chemotherapy in advanced gastric cancer. Meta-analysis of randomized trials [6]
- Research article The Mesenteric Fat and Intestinal Muscle Interface: Creeping Fat Influencing Stricture Formation in Crohn's Disease [7]
- Research article The peritoneal "soil" for a cancerous "seed": a comprehensive review of the pathogenesis of intraperitoneal cancer metastases [8]
- Research article The histophysiology and pathophysiology of the peritoneum [9]
- Research article Peritoneal adhesions: Occurrence, prevention and experimental models [10]
References
- Fischer A, Wannemacher J, Christ S, Koopmans T, Kadri S, Zhao J, et al.. Neutrophils direct preexisting matrix to initiate repair in damaged tissues. . 2022. PMID 35354953 · DOI · PMC8986538
- Terri M, Trionfetti F, Montaldo C, Cordani M, Tripodi M, Lopez-Cabrera M, et al.. Mechanisms of Peritoneal Fibrosis: Focus on Immune Cells-Peritoneal Stroma Interactions. . 2021. PMID 33854496 · DOI · PMC8039516
- Jin H, Liu K, Tang J, Huang X, Wang H, Zhang Q, et al.. Genetic fate-mapping reveals surface accumulation but not deep organ invasion of pleural and peritoneal cavity macrophages following injury. . 2021. PMID 34001904 · DOI · PMC8129080
- Rahmana MDR, Hill CJ, Wilm B, Hapangama DK. Compound design of a patient-derived 3D cell culture system modelling early peritoneal endometriosis. . 2026. PMID 41392657 · DOI · PMC12919959
- Coffey JC, O'Leary DP. The mesentery: structure, function, and role in disease. Lancet Gastroenterol Hepatol. 2016. PMID 28404096 · DOI
- Coccolini F, Cotte E, Glehen O, Lotti M, Poiasina E, Catena F, et al.. Intraperitoneal chemotherapy in advanced gastric cancer. Meta-analysis of randomized trials. Eur J Surg Oncol. 2014. PMID 24290371 · DOI
- Mao R, Kurada S, Gordon IO, Baker ME, Gandhi N, McDonald C, et al.. The Mesenteric Fat and Intestinal Muscle Interface: Creeping Fat Influencing Stricture Formation in Crohn's Disease. Inflamm Bowel Dis. 2019. PMID 30346528 · DOI
- Mikuła-Pietrasik J, Uruski P, Tykarski A, Książek K. The peritoneal "soil" for a cancerous "seed": a comprehensive review of the pathogenesis of intraperitoneal cancer metastases. Cell Mol Life Sci. 2018. PMID 28956065 · DOI · PMC5765197
- van Baal JO, Van de Vijver KK, Nieuwland R, van Noorden CJ, van Driel WJ, Sturk A, et al.. The histophysiology and pathophysiology of the peritoneum. Tissue Cell. 2017. PMID 27890350 · DOI
- Tang J, Xiang Z, Bernards MT, Chen S. Peritoneal adhesions: Occurrence, prevention and experimental models. Acta Biomater. 2020. PMID 32871282 · DOI
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.