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New insights in the control of vascular permeability: vascular endothelial-cadherin and other players
Abstract
PURPOSE OF REVIEW: The control of the endothelial barrier function is essential for vascular homeostasis and is mainly mediated by cell-to-cell junctions that tightly regulate permeability to plasma solutes and circulating cells such as leukocytes and tumor cells. While in some circumstances the transient dismantling of endothelial cell junctions might be beneficial, in pathological conditions, such as cancer, severe alterations of endothelial junction composition and function are detrimental, causing massive edema and increased interstitial pressure. Here, we aim to discuss the newly and most recently identified molecular mechanisms that cooperate in the control of vascular permeability. RECENT FINDINGS: Although the involvement of vascular endothelial-cadherin in the regulation of vascular leakage is well known, recent findings shed light on additional molecules involved in the control of vascular endothelial-cadherin phosphorylation in physiological and pathological conditions, and identified new unknown regulators of the endothelial barrier function. SUMMARY: In the past years, several studies explored the contribution of various signaling pathways in the regulation of vascular leakage. Despite encouraging results, a more comprehensive understanding of the molecular mechanisms involved in this process will define druggable targets for new therapeutic interventions to limit endothelial barrier dysfunctions.
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“These inflammatory agents activate signals that converge on common downstream pathways, including dismantling of vascular endothelial (VE)-cadherin (Cadherin 5, CDH5) from EC–EC junctions (4, 5).”
From Targeting β1-integrin inhibits vascular leakage in endotoxemia (2018) · cites this paper as [5]
In the citing paper
“Proinflammatory cytokines, microbial components such as lipopolysaccharide (LPS), thrombin, and vascular endothelial growth factor (VEGF) induce endothelial permeability by binding to their cognate receptors on ECs.”
From Targeting β1-integrin inhibits vascular leakage in endotoxemia (2018) · cites this paper as [5]
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Research works printed but not linked: 1
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Cited by
Sorted by citations
Targeting β1-integrin inhibits vascular leakage in endotoxemia
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“translocation of alpha(5)beta(1) integrins promotes early fibronectin fibrillogenesis.”
Background
Metadata
- Authors
- Trani, M., & Dejana, E.
- Affiliations
- University of Milan (IT)
- Corresponding author
- Dejana, Elisabetta
- ORCID
- Dejana, Elisabetta
- Venue
- Current Opinion in Hematology
- Published
- 2015-05
- Volume
- 22
- Issue
- 3
- Pages
- 267-272
- ISSN
- 1065-6251 (ISSN-L)
- OpenAlex
- W2039344188
- Cited by
- 52
- References
- 40
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 2 · 2022: 3 · 2021: 5 · 2020: 10 · 2019: 9 · 2018: 6 · 2017: 7 · 2016: 4 · 2015: 2
- FWCI
- 0.51
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Hematology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Associazione Italiana per la Ricerca sul Cancro
- Topics
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Keywords
- vascular permeability, endothelial barrier function, endothelial junctions, VE-cadherin, vascular leakage, leukocyte transendothelial migration, tumor cell extravasation, edema, interstitial fluid pressure, vascular homeostasis, signaling pathways, therapeutic target
- MeSH terms
- Capillary Permeability, Endothelium, Vascular, Humans, Signal Transduction
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