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 (612 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
The layers of epithelial cells which cover the inner and outer surfaces of the cutaneous, mucus, and serous tissues and glands of the body.
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: Epithelial Tissue; Epithelial Tissues; Tissue, Epithelial; Tissues, Epithelial; Mesothelium; Mesothelial Tissue; Mesothelial Tissues; Tissue, Mesothelial.
Where it fits in the MeSH classification
- Broader topics
- Tissues
- Narrower topics
- Endothelium; Epidermis; Epithelium, Corneal; Pigment Epithelium of Eye; Seminiferous Epithelium; Urothelium
Related concepts
- Epithelial Cells
Research landscape
PubMed indexes 253,928 records tagged with the MeSH heading “Epithelium” (counts retrieved 2026-10-31). 21,344 of them (8.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 118,612 records.
Reviews account for 28,450 records (11.2%) and meta-analyses for 360. Randomized controlled trials number 3,991 (1.6%) 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 | 118,612 |
| 2000-2009 | 64,729 |
| 2010-2019 | 49,243 |
| 2020 onward | 21,344 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 28,450 | 11.2% |
| Meta-analyses | 360 | 0.1% |
| Randomized controlled trials | 3,991 | 1.6% |
Method: PubMed query "Epithelium"[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 |
|---|---|---|---|---|
| Senolytic Treatment With Fisetin Reverses Age-Related Endothelial Dysfunction Partially Mediated by SASP Factor CXCL12 | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 42021544 · DOI · PMC13103471 |
| Hyperglycemia-Induced Endothelial Dysfunction: From Classical Pathogenetic Mechanisms to Emerging Insights into ACE2 Protective Action | 2026 | Review article Design not recorded in structured metadata | 5 | cc by PMID 41898523 · DOI · PMC13026142 |
| Endothelial cannabinoid CB1 receptor deficiency reduces shear stress-induced arterial inflammation and lipid uptake | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42414306 · DOI · PMC13342577 |
Senolytic Treatment With Fisetin Reverses Age-Related Endothelial Dysfunction Partially Mediated by SASP Factor CXCL12 [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Advancing age is the strongest risk factor for cardiovascular diseases (CVDs), primarily due to progressive vascular endothelial dysfunction.
- Closing excerpt
- These results identify the SASP and CXCL12 as drivers of age-related endothelial dysfunction and establish mechanisms of senolytic intervention with fisetin supplementation.
- 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 (253 words)
Advancing age is the strongest risk factor for cardiovascular diseases (CVDs), primarily due to progressive vascular endothelial dysfunction. Cellular senescence and the senescence-associated secretory phenotype (SASP) contribute to age-related endothelial dysfunction by promoting mitochondrial oxidative stress and inflammation, which reduce nitric oxide (NO) bioavailability. However, the molecular changes in senescent endothelial cells (ECs) and their role in endothelial dysfunction with aging remain unclear. As such, we sought to identify the EC-related signaling pathways, endothelial-associated SASP factors, and their impact on endothelial function with aging. Single-cell transcriptomics was performed on aortas from young (6mos) and old (27mos) female and male mice with and without in vivo senolytic treatment with fisetin (100 mg/kg/day administered intermittently) to characterize EC senescence and transcript expression changes. Circulating levels of SASP factors were measured to assess systemic changes associated with aging and fisetin treatment. Plasma exposure experiments were conducted in isolated mouse arteries and cultured human aortic ECs to determine the causal role of the circulating SASP milieu and specific SASP factors in mediating endothelial dysfunction and underlying mechanisms of action. Senescent ECs exhibited elevated expression of SASP factors, particularly Cxcl12, which was reversed by fisetin supplementation, with responses also reflected in circulating CXCL12 concentrations. Plasma from old mice impaired endothelial function by inducing vascular cell senescence, reducing NO, increasing mitochondrial oxidative stress, shifting receptor and promoting endothelial-to-mesenchymal transition-effects partially driven by CXCL12 and prevented by fisetin. These results identify the SASP and CXCL12 as drivers of age-related endothelial dysfunction and establish mechanisms of senolytic intervention with fisetin supplementation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42021544 · DOI · PMC13103471
Hyperglycemia-Induced Endothelial Dysfunction: From Classical Pathogenetic Mechanisms to Emerging Insights into ACE2 Protective Action [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Diabetes is a pivotal risk factor for cardiovascular disease as well as microvascular complications, including retinopathy and nephropathy.
- Closing excerpt
- In turn, understanding the molecular interconnections between hyperglycemia and endothelial dysfunction is crucial for developing novel strategies to restore endothelial homeostasis and mitigate diabetic vascular complications.
- 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 (225 words)
Diabetes is a pivotal risk factor for cardiovascular disease as well as microvascular complications, including retinopathy and nephropathy. Chronic hyperglycemia is a key player in linking diabetes with endothelial dysfunction which, in turn, contributes to cardiovascular disease. Indeed, hyperglycemia acts as a trigger for endothelial dysfunction, promoting a shift in the endothelium from a protective, anti-inflammatory state to a dysfunctional, injury-prone phenotype. A hyperglycemic environment triggers several pathogenetic mechanisms, including alterations in bioenergetics, production of advanced glycation end products, oxidative stress and mitochondrial dysfunction, all contributing to endothelial dysfunction. The activation of these pathophysiological mechanisms by hyperglycemia culminates in reduced nitric oxide production, as well as the induction of oxidative stress and inflammation, all of which are pivotal in impairing endothelial homeostasis and promoting cellular damage. Besides these classical mechanisms, there is growing attention on novel pathogenetic factors linking diabetic hyperglycemia with endothelial dysfunction, such as the ACE2 protein. The latter is emergeing for its potential to counter hyperglycemia-induced cellular damage through its vasoprotective and anti-inflammatory actions, making it a promising therapeutic target for tackling endothelial dysfunction. This review provides an overview of classical as well as emerging mechanisms underpinning the deleterious effects of diabetic hyperglycemia on endothelial dysfunction. In turn, understanding the molecular interconnections between hyperglycemia and endothelial dysfunction is crucial for developing novel strategies to restore endothelial homeostasis and mitigate diabetic vascular complications.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41898523 · DOI · PMC13026142
Endothelial cannabinoid CB1 receptor deficiency reduces shear stress-induced arterial inflammation and lipid uptake [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Peripheral cannabinoid CB1 receptor antagonists that lack central nervous system effects are emerging as promising therapies for metabolic disease, yet the role of endothelial CB1 signaling in atherosclerosis remains unclear.
- Closing excerpt
- These findings identify endothelial CB1 as a proatherogenic, sex-biased regulator of vascular lipid transport and plaque development and associated metabolic dysfunction.
- 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 (134 words)
Peripheral cannabinoid CB1 receptor antagonists that lack central nervous system effects are emerging as promising therapies for metabolic disease, yet the role of endothelial CB1 signaling in atherosclerosis remains unclear. Here, we show that endothelial CB1 is expressed in human atherosclerotic plaques, is induced by oscillatory shear stress in atheroprone flow regions, and promotes vascular inflammation, permeability and lipid uptake. Endothelial-specific Cnr1 deletion or peripheral CB1 antagonism in mice attenuates atherosclerosis, reduces endothelial caveolae-dependent low-density lipoprotein uptake by downregulating caveolin-1 and ALK1 expression, and improves metabolic parameters in brown and white adipose tissue and the liver. The anti-atherogenic and metabolic effects are more pronounced in females, which is possibly linked to estrogen signaling. These findings identify endothelial CB1 as a proatherogenic, sex-biased regulator of vascular lipid transport and plaque development and associated metabolic dysfunction.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42414306 · DOI · PMC13342577
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 Flavonoids, flavonoid-rich foods, and cardiovascular risk: a meta-analysis of randomized controlled trials [4]
- Research article Prognostic Value of Flow-Mediated Vasodilation in Brachial Artery and Fingertip Artery for Cardiovascular Events: A Systematic Review and Meta-Analysis [5]
- Research article Mediterranean dietary pattern, inflammation and endothelial function: a systematic review and meta-analysis of intervention trials [6]
- Research article Exercise modalities and endothelial function: a systematic review and dose-response meta-analysis of randomized controlled trials [7]
- Research article Non-invasive endothelial function testing and the risk of adverse outcomes: a systematic review and meta-analysis [8]
- Research article Effects of Olive Oil on Markers of Inflammation and Endothelial Function-A Systematic Review and Meta-Analysis [9]
References
- Mahoney SA, Mazan-Mamczarz K, Tsitsipatis D, VanDongen NS, Henry-Smith C, Okereke AN, et al.. Senolytic Treatment With Fisetin Reverses Age-Related Endothelial Dysfunction Partially Mediated by SASP Factor CXCL12. . 2026. PMID 42021544 · DOI · PMC13103471
- Lodi G, Sergi D, Dipinto A, Bompan F, Secchiero P, Voltan R, et al.. Hyperglycemia-Induced Endothelial Dysfunction: From Classical Pathogenetic Mechanisms to Emerging Insights into ACE2 Protective Action. . 2026. PMID 41898523 · DOI · PMC13026142
- Chen B, Prabhu A, Li G, Kaltenbach A, Wang Y, Shakir G, et al.. Endothelial cannabinoid CB1 receptor deficiency reduces shear stress-induced arterial inflammation and lipid uptake. . 2026. PMID 42414306 · DOI · PMC13342577
- Hooper L, Kroon PA, Rimm EB, Cohn JS, Harvey I, Le Cornu KA, et al.. Flavonoids, flavonoid-rich foods, and cardiovascular risk: a meta-analysis of randomized controlled trials. Am J Clin Nutr. 2008. PMID 18614722 · DOI
- Matsuzawa Y, Kwon TG, Lennon RJ, Lerman LO, Lerman A. Prognostic Value of Flow-Mediated Vasodilation in Brachial Artery and Fingertip Artery for Cardiovascular Events: A Systematic Review and Meta-Analysis. J Am Heart Assoc. 2015. PMID 26567372 · DOI · PMC4845238
- Schwingshackl L, Hoffmann G. Mediterranean dietary pattern, inflammation and endothelial function: a systematic review and meta-analysis of intervention trials. Nutr Metab Cardiovasc Dis. 2014. PMID 24787907 · DOI
- Ashor AW, Lara J, Siervo M, Celis-Morales C, Oggioni C, Jakovljevic DG, et al.. Exercise modalities and endothelial function: a systematic review and dose-response meta-analysis of randomized controlled trials. Sports Med. 2015. PMID 25281334 · DOI
- Xu Y, Arora RC, Hiebert BM, Lerner B, Szwajcer A, McDonald K, et al.. Non-invasive endothelial function testing and the risk of adverse outcomes: a systematic review and meta-analysis. Eur Heart J Cardiovasc Imaging. 2014. PMID 24399339 · DOI
- Schwingshackl L, Christoph M, Hoffmann G. Effects of Olive Oil on Markers of Inflammation and Endothelial Function-A Systematic Review and Meta-Analysis. Nutrients. 2015. PMID 26378571 · DOI · PMC4586551
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.