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 (713 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
A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities 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: Endotheliums.
Where it fits in the MeSH classification
- Broader topics
- Epithelium
- Narrower topics
- Endothelium, Corneal; Endothelium, Lymphatic; Endothelium, Vascular; Pericytes
Related concepts
- Endothelium
- Vascular
- Lymphatic
Research landscape
PubMed indexes 126,861 records tagged with the MeSH heading “Endothelium” (counts retrieved 2026-10-31). 10,144 of them (8.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 49,048 records.
Reviews account for 17,990 records (14.2%) and meta-analyses for 268. Randomized controlled trials number 3,083 (2.4%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 49,048 |
| 2000-2009 | 41,011 |
| 2010-2019 | 26,658 |
| 2020 onward | 10,144 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 17,990 | 14.2% |
| Meta-analyses | 268 | 0.2% |
| Randomized controlled trials | 3,083 | 2.4% |
Method: PubMed query "Endothelium"[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 |
|---|---|---|---|---|
| Vascular Complications of Long COVID-From Endothelial Dysfunction to Systemic Thrombosis: A Systematic Review | 2025 | Systematic review Design not recorded in structured metadata | 23 | cc by PMID 41516301 · DOI · PMC12786942 |
| Flavivirus NS1-triggered endothelial dysfunction promotes virus dissemination | 2025 | Research article Design not recorded in structured metadata | 15 | cc by PMID 41474801 · DOI · PMC12779140 |
| CD146+ pericyte-like lung cancer brain metastatic stem cells promote tumor angiogenesis through dual regulatory effects on the VEGF/VEGFR axis | 2026 | Research article Design not recorded in structured metadata | 8 | cc by PMID 41356185 · DOI · PMC12680595 |
Vascular Complications of Long COVID-From Endothelial Dysfunction to Systemic Thrombosis: A Systematic Review [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is associated not only with respiratory illness but also with profound vascular and coagulation disturbances.
- Closing excerpt
- This review synthesizes current evidence on vascular complications in LC, highlighting endothelial dysfunction as a central pathophysiological nexus linking the acute phase of SARS-CoV-2 infection with chronic LC manifestations.
- 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 (192 words)
Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is associated not only with respiratory illness but also with profound vascular and coagulation disturbances. Long COVID (LC) is characterized by persistent symptoms such as fatigue, dyspnea, cognitive impairment, and palpitations. Mechanistically, SARS-CoV-2 induces direct endothelial injury, promotes a pro-inflammatory cytokine milieu, and activates platelets, leading to immunothrombosis and impaired fibrinolysis. Consequently, patients exhibit microthrombosis, elevated plasma D-dimer, fibrinogen dysregulation, and persistent hypercoagulability. Clinically, this translates into an increased risk of venous thromboembolism, including deep vein thrombosis and pulmonary embolism, as well as arterial thrombotic events such as myocardial infarction and stroke, which may persist months after acute infection. Understanding the interplay between endothelial injury, inflammation, and coagulation is crucial for risk stratification and the development of preventive and therapeutic strategies. We conducted a systematic narrative review of the literature, including human clinical and mechanistic studies identified through PubMed, Scopus and Web of Science up to 30 September 2025. This review synthesizes current evidence on vascular complications in LC, highlighting endothelial dysfunction as a central pathophysiological nexus linking the acute phase of SARS-CoV-2 infection with chronic LC manifestations.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41516301 · DOI · PMC12786942
Flavivirus NS1-triggered endothelial dysfunction promotes virus dissemination [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The Flaviviridae are a family of viruses that include the important arthropod-borne human pathogens dengue virus, West Nile virus, Zika virus, Japanese encephalitis virus, and yellow fever virus.
- Closing excerpt
- Taken together, our study indicates that flavivirus NS1 acts as a viral toxin and promotes virus dissemination across endothelial barriers, providing an evolutionary basis for virus-triggered vascular leak.
- 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 (252 words)
The Flaviviridae are a family of viruses that include the important arthropod-borne human pathogens dengue virus, West Nile virus, Zika virus, Japanese encephalitis virus, and yellow fever virus. Flavivirus nonstructural protein 1 (NS1) is essential for virus replication but is also secreted from virus-infected cells. Extracellular NS1 acts as a virulence factor during flavivirus infection in multiple ways, including triggering endothelial dysfunction and vascular leak via interaction with endothelial cells. While the role of NS1 in inducing vascular leak and exacerbating pathogenesis is well appreciated, if and how NS1-triggered endothelial dysfunction promotes virus infection remains obscure. Flaviviruses have a common need to disseminate from circulation into specific tissues where virus-permissive cells reside. Tissue-specific dissemination is associated with disease manifestations of a given flavivirus, but mechanisms dictating virus dissemination are unclear. Here we show that NS1-mediated endothelial dysfunction promotes virus dissemination in vitro and in vivo. In mouse models of dengue virus infection, we show that anti-NS1 antibodies decrease virus dissemination, while the addition of exogenous NS1 promotes virus dissemination. Using an in vitro system, we show that NS1 promotes virus dissemination in two distinct ways: (1) promoting crossing of barriers and (2) increasing infectivity of target cells in a tissue- and virus-specific manner. The capacity of NS1 to modulate infectivity correlates with a physical association between virions and NS1, suggesting a potential NS1-virion interaction. Taken together, our study indicates that flavivirus NS1 acts as a viral toxin and promotes virus dissemination across endothelial barriers, providing an evolutionary basis for virus-triggered vascular leak.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41474801 · DOI · PMC12779140
CD146+ pericyte-like lung cancer brain metastatic stem cells promote tumor angiogenesis through dual regulatory effects on the VEGF/VEGFR axis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Rationale: Anti-angiogenic therapy is indispensable for the treatment of non-small cell lung carcinoma (NSCLC)-derived brain metastasis (BrM).
- Closing excerpt
- Conclusions: CD146+ BrM-CSCs promotes high vascularization of lung cancer brain metastases through dual enhancement of VEGF/VEFGR, which suggests that targeting CD146 is a novel anti-vascular strategy for BrM.
- 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 (269 words)
Rationale: Anti-angiogenic therapy is indispensable for the treatment of non-small cell lung carcinoma (NSCLC)-derived brain metastasis (BrM). Targeting vascular endothelial growth factor (VEGF) and its receptor (VEGFR) is the most effective strategy against angiogenesis. However, bevacizumab (Bev) shows limited therapeutic effects on NSCLC BrM. The plasticity of cancer stem cells (CSCs) has been found to drive therapeutic resistance via the "mimicry" behavior. Methods: CD146+ BrM-CSCs were validated in clinical tissues and organoids using immunostaining assays. The ability of CD146+ BrM-CSCs to induce angiogenesis was examined using an ex vivo multi-organ microfluidic bionic chip and animal models. The effects of CD146 on the VEGF and VEGFR were investigated by RNA-sequencing, molecular dynamics simulation and further cellular and clinical validations. Mechanisms of CD146 upregulation in the brain microenvironment were explored by proteomics, luciferase reporter assay and immunoprecipitation. The anti-vascular efficacy of drugs targeting CD146 on BrM was evaluated in animal studies. Results: BrM-CSCs mimic the pericytes to promote tumor angiogenesis by acquired high expression of CD146 in the brain tumor microenvironment. CD146 exert a dual promotive effect on VEGF/VEGFR2 axis by both up-regulating tumoral VEGF transcription and stabilizing and sensitizing VEGFR2 on endothelial cells as a co-receptor. Secretion of growth arrest specific 6 (GAS6) by the reactive astrocytes led to the CD146 upregulation by activating AXL. Targeting CD146 by imaprelimab or AXL by bemcentinib exhibits more effective anti-angiogenic effects than Bev for BrM in vivo. These findings provide novel anti-vascular strategies for BrM. Conclusions: CD146+ BrM-CSCs promotes high vascularization of lung cancer brain metastases through dual enhancement of VEGF/VEFGR, which suggests that targeting CD146 is a novel anti-vascular strategy for BrM.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41356185 · DOI · PMC12680595
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 Prognostic Value of Flow-Mediated Vasodilation in Brachial Artery and Fingertip Artery for Cardiovascular Events: A Systematic Review and Meta-Analysis [4]
- Research article Mediterranean dietary pattern, inflammation and endothelial function: a systematic review and meta-analysis of intervention trials [5]
- Research article Exercise modalities and endothelial function: a systematic review and dose-response meta-analysis of randomized controlled trials [6]
- Research article Non-invasive endothelial function testing and the risk of adverse outcomes: a systematic review and meta-analysis [7]
- Research article Effects of Olive Oil on Markers of Inflammation and Endothelial Function-A Systematic Review and Meta-Analysis [8]
- Research article Exercise training and endothelial function in patients with type 2 diabetes: a meta-analysis [9]
References
- Stojanovic M, Djuric M, Nenadic I, Bojic S, Andrijevic A, Popovic A, et al.. Vascular Complications of Long COVID-From Endothelial Dysfunction to Systemic Thrombosis: A Systematic Review. . 2025. PMID 41516301 · DOI · PMC12786942
- Puerta-Guardo H, Biering SB, Castillo-Rojas B, DiBiasio-White MJ, Lo NTN, Espinosa DA, et al.. Flavivirus NS1-triggered endothelial dysfunction promotes virus dissemination. . 2025. PMID 41474801 · DOI · PMC12779140
- Liu W, Duan W, Xia S, Liu Y, Chu H, Liang K, et al.. CD146+ pericyte-like lung cancer brain metastatic stem cells promote tumor angiogenesis through dual regulatory effects on the VEGF/VEGFR axis. . 2026. PMID 41356185 · DOI · PMC12680595
- 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
- Qiu S, Cai X, Yin H, Sun Z, Zügel M, Steinacker JM, et al.. Exercise training and endothelial function in patients with type 2 diabetes: a meta-analysis. Cardiovasc Diabetol. 2018. PMID 29720185 · DOI · PMC5930739
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.