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 (622 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
The property of blood capillary endothelium that allows for the selective exchange of substances between the blood and surrounding tissues and through membranous barriers such as the blood-air barrier; blood-aqueous barrier; blood-brain barrier; blood-nerve barrier; blood-retinal barrier; and blood-testis barrier. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (tight junctions) which may limit large molecule movement.
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: Permeability, Capillary; Capillary Permeabilities; Permeabilities, Capillary; Permeability, Microvascular; Microvascular Permeability; Microvascular Permeabilities; Permeabilities, Microvascular; Vascular Permeability.
Where it fits in the MeSH classification
- Broader topics
- Biological Transport; Cardiovascular Physiological Phenomena
- See also
- Blood-Brain Barrier; Blood-Retinal Barrier; Blood-Testis Barrier; Blood-Air Barrier; Blood-Aqueous Barrier; Capillary Leak Syndrome; Blood-Nerve Barrier; Transendothelial and Transepithelial Migration
Related concepts
- Endothelium
- Blood-Air Barrier
- Blood-Aqueous Barrier
- Blood-Brain Barrier
- Blood-Nerve Barrier
- Blood-Retinal Barrier
- Blood-Testis Barrier
- Tight Junctions
Research landscape
PubMed indexes 22,569 records tagged with the MeSH heading “Capillary Permeability” (counts retrieved 2026-10-29). 1,218 of them (5.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 13,327 records.
Reviews account for 2,178 records (9.7%) and meta-analyses for 5. Randomized controlled trials number 127 (0.6%) 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 | 13,327 |
| 2000-2009 | 3,851 |
| 2010-2019 | 4,173 |
| 2020 onward | 1,218 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,178 | 9.7% |
| Meta-analyses | 5 | 0.0% |
| Randomized controlled trials | 127 | 0.6% |
Method: PubMed query "Capillary Permeability"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cardiovascular medicine
Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.
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 |
|---|---|---|---|---|
| Role of Angiopoietin-2 in Vascular Physiology and Pathophysiology | 2019 | Review article Design not recorded in structured metadata | 441 | cc by PMID 31108880 · DOI · PMC6562915 |
| The vascular endothelium: the cornerstone of organ dysfunction in severe SARS-CoV-2 infection | 2020 | Review article Design not recorded in structured metadata | 364 | cc by PMID 32546188 · DOI · PMC7296907 |
| Regulation and Dysregulation of Endothelial Permeability during Systemic Inflammation | 2022 | Review article Design not recorded in structured metadata | 157 | cc by PMID 35741064 · DOI · PMC9221661 |
| Zebrafish macrophages convert physical wound signals into rapid vascular permeabilization | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 41651853 · DOI · PMC12916771 |
Role of Angiopoietin-2 in Vascular Physiology and Pathophysiology [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Angiopoietins 1-4 (Ang1-4) represent an important family of growth factors, whose activities are mediated through the tyrosine kinase receptors, Tie1 and Tie2.
- Closing excerpt
- In this review, we summarize the activity of Ang2 on blood and lymphatic endothelial cells, its significance in human physiology and disease, and provide a current view of the molecular signaling pathways regulated by Ang2 in endothelial cells.
- 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 (123 words)
Angiopoietins 1-4 (Ang1-4) represent an important family of growth factors, whose activities are mediated through the tyrosine kinase receptors, Tie1 and Tie2. The best characterized are angiopoietin-1 (Ang1) and angiopoietin-2 (Ang2). Ang1 is a potent angiogenic growth factor signaling through Tie2, whereas Ang2 was initially identified as a vascular disruptive agent with antagonistic activity through the same receptor. Recent data demonstrates that Ang2 has context-dependent agonist activities. Ang2 plays important roles in physiological processes and the deregulation of its expression is characteristic of several diseases. In this review, we summarize the activity of Ang2 on blood and lymphatic endothelial cells, its significance in human physiology and disease, and provide a current view of the molecular signaling pathways regulated by Ang2 in endothelial cells.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31108880 · DOI · PMC6562915
The vascular endothelium: the cornerstone of organ dysfunction in severe SARS-CoV-2 infection [2]
Abstract reading summary — source excerpts
- Opening excerpt
- In severe SARS-CoV-2 infections, emerging data including recent histopathological studies have emphasized the crucial role of endothelial cells (ECs) in vascular dysfunction, immunothrombosis, and inflammation.
- Closing excerpt
- Studies focusing on endothelial dysfunction in COVID-19 patients are warranted as to decipher their precise role in severe SARS-CoV-2 infection and organ dysfunction and to identify targets for further interventions.
- 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 (176 words)
In severe SARS-CoV-2 infections, emerging data including recent histopathological studies have emphasized the crucial role of endothelial cells (ECs) in vascular dysfunction, immunothrombosis, and inflammation.Histopathological studies have evidenced direct viral infection of ECs, endotheliitis with diffuse endothelial inflammation, and micro- and macrovascular thrombosis both in the venous and arterial circulations. Venous thrombotic events, particularly pulmonary embolism, with elevated D-dimer and coagulation activation are highly prevalent in COVID-19 patients. The pro-inflammatory cytokine storm, with elevated levels of interleukin-6 (IL-6), IL-2 receptor, and tumor necrosis factor-α, could also participate in endothelial dysfunction and leukocyte recruitment in the microvasculature. COVID-19-induced endotheliitis may explain the systemic impaired microcirculatory function in different organs in COVID-19 patients. Ongoing trials directly and indirectly target COVID-19-related endothelial dysfunctions: i.e., a virus-cell entry using recombinant angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS-2) blockade, coagulation activation, and immunomodulatory therapies, such as anti-IL-6 strategies. Studies focusing on endothelial dysfunction in COVID-19 patients are warranted as to decipher their precise role in severe SARS-CoV-2 infection and organ dysfunction and to identify targets for further interventions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32546188 · DOI · PMC7296907
Regulation and Dysregulation of Endothelial Permeability during Systemic Inflammation [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Systemic inflammation can be triggered by infection, surgery, trauma or burns.
- Closing excerpt
- In this review, we provide a comprehensive summary of the major players, such as the angiopoietin-Tie2 signaling axis, adrenomedullin and vascular endothelial (VE-) cadherin, that substantially contribute to the regulation and dysregulation of endothelial permeability during systemic inflammation and elucidate treatment strategies targeting the preservation of vascular integrity.
- 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 (200 words)
Systemic inflammation can be triggered by infection, surgery, trauma or burns. During systemic inflammation, an overshooting immune response induces tissue damage resulting in organ dysfunction and mortality. Endothelial cells make up the inner lining of all blood vessels and are critically involved in maintaining organ integrity by regulating tissue perfusion. Permeability of the endothelial monolayer is strictly controlled and highly organ-specific, forming continuous, fenestrated and discontinuous capillaries that orchestrate the extravasation of fluids, proteins and solutes to maintain organ homeostasis. In the physiological state, the endothelial barrier is maintained by the glycocalyx, extracellular matrix and intercellular junctions including adherens and tight junctions. As endothelial cells are constantly sensing and responding to the extracellular environment, their activation by inflammatory stimuli promotes a loss of endothelial barrier function, which has been identified as a hallmark of systemic inflammation, leading to tissue edema formation and hypotension and thus, is a key contributor to lethal outcomes. In this review, we provide a comprehensive summary of the major players, such as the angiopoietin-Tie2 signaling axis, adrenomedullin and vascular endothelial (VE-) cadherin, that substantially contribute to the regulation and dysregulation of endothelial permeability during systemic inflammation and elucidate treatment strategies targeting the preservation of vascular integrity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35741064 · DOI · PMC9221661
Zebrafish macrophages convert physical wound signals into rapid vascular permeabilization [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Blood vessels near injury sites rapidly dilate, become permeable, and release serum and leukocytes into the wounded tissue to support healing and regeneration.
- Closing excerpt
- By revealing a previously undescribed physiological function of nuclear membrane mechanotransduction, we provide real-time insights into the long-range communication of wounds and blood vessels in intact tissue.
- 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 (123 words)
Blood vessels near injury sites rapidly dilate, become permeable, and release serum and leukocytes into the wounded tissue to support healing and regeneration. How the vasculature senses distant homeostatic tissue perturbations within seconds-to-minutes remains incompletely understood. Using high-speed imaging of live zebrafish larvae, we monitor two hallmark vascular responses to injury: vessel dilation and serum exudation. By genetic, pharmacologic, and osmotic perturbation along with leukocyte depletion, we show that the cPla2 nuclear membrane mechanotransduction pathway converts a ~ 50 μm/s osmotic wound signal into rapid vessel-permeabilization via perivascular macrophages, 5-lipoxygenase (Alox5a), and leukotriene A4 hydrolase (Lta4h). By revealing a previously undescribed physiological function of nuclear membrane mechanotransduction, we provide real-time insights into the long-range communication of wounds and blood vessels in intact tissue.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41651853 · DOI · PMC12916771
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 Vascular permeability factor/vascular endothelial growth factor, microvascular hyperpermeability, and angiogenesis [5]
- Research article Signaling mechanisms regulating endothelial permeability [6]
- Research article Astrocyte-endothelial interactions and blood-brain barrier permeability [7]
- Research article Cytoskeletal regulation of pulmonary vascular permeability [8]
- Research article Microvascular fluid exchange and the revised Starling principle [9]
- Research article Microvascular permeability [10]
References
- Akwii RG, Sajib MS, Zahra FT, Mikelis CM. Role of Angiopoietin-2 in Vascular Physiology and Pathophysiology. . 2019. PMID 31108880 · DOI · PMC6562915
- Pons S, Fodil S, Azoulay E, Zafrani L. The vascular endothelium: the cornerstone of organ dysfunction in severe SARS-CoV-2 infection. . 2020. PMID 32546188 · DOI · PMC7296907
- Hellenthal KEM, Brabenec L, Wagner NM. Regulation and Dysregulation of Endothelial Permeability during Systemic Inflammation. . 2022. PMID 35741064 · DOI · PMC9221661
- Gelashvili Z, Shen Z, Ma Y, Jelcic M, Niethammer P. Zebrafish macrophages convert physical wound signals into rapid vascular permeabilization. . 2026. PMID 41651853 · DOI · PMC12916771
- Dvorak HF, Brown LF, Detmar M, Dvorak AM. Vascular permeability factor/vascular endothelial growth factor, microvascular hyperpermeability, and angiogenesis. Am J Pathol. 1995. PMID 7538264 · PMC1869291
- Mehta D, Malik AB. Signaling mechanisms regulating endothelial permeability. Physiol Rev. 2006. PMID 16371600 · DOI
- Abbott NJ. Astrocyte-endothelial interactions and blood-brain barrier permeability. J Anat. 2002. PMID 12162730 · DOI
- Dudek SM, Garcia JG. Cytoskeletal regulation of pulmonary vascular permeability. J Appl Physiol (1985). 2001. PMID 11568129 · DOI
- Levick JR, Michel CC. Microvascular fluid exchange and the revised Starling principle. Cardiovasc Res. 2010. PMID 20200043 · DOI
- Michel CC, Curry FE. Microvascular permeability. Physiol Rev. 1999. PMID 10390517 · 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 2026-10-29.
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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.