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 (778 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 specialized transport barrier, in the EYE, formed by the retinal pigment epithelium, and the endothelium of the blood vessels of the retina. tight junctions joining adjacent cells keep the barrier between cells continuous.
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: Barrier, Blood-Retinal; Barriers, Blood-Retinal; Blood Retinal Barrier; Blood-Retinal Barriers; Retinal-Blood Barrier; Barrier, Retinal-Blood; Barriers, Retinal-Blood; Retinal Blood Barrier.
Where it fits in the MeSH classification
- Broader topics
- Cardiovascular System; Retina
- See also
- Capillary Permeability
Related concepts
- Epithelium
- Endothelium
- Blood Vessels
- Retina
- Tight Junctions
Research landscape
PubMed indexes 1,751 records tagged with the MeSH heading “Blood-Retinal Barrier” (counts retrieved 2026-10-31). 371 of them (21.2%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 611 records.
Reviews account for 291 records (16.6%) and meta-analyses for 1. Randomized controlled trials number 30 (1.7%) 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 | 410 |
| 2000-2009 | 359 |
| 2010-2019 | 611 |
| 2020 onward | 371 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 291 | 16.6% |
| Meta-analyses | 1 | 0.1% |
| Randomized controlled trials | 30 | 1.7% |
Method: PubMed query "Blood-Retinal Barrier"[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 |
|---|---|---|---|---|
| The Role of Microglia in Diabetic Retinopathy: Inflammation, Microvasculature Defects and Neurodegeneration | 2018 | Review article Design not recorded in structured metadata | 340 | cc by PMID 29301251 · DOI · PMC5796059 |
| Plastic roles of pericytes in the blood-retinal barrier | 2017 | Research article Design not recorded in structured metadata | 279 | cc by PMID 28508859 · DOI · PMC5440855 |
| A novel transgenic zebrafish model for blood-brain and blood-retinal barrier development | 2010 | Research article Design not recorded in structured metadata | 197 | cc by PMID 20653957 · DOI · PMC2914679 |
| Chronic dental lighting disrupts blood-retinal barrier homeostasis via vascular and inflammatory pathways | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 41680131 · DOI · PMC12902021 |
The Role of Microglia in Diabetic Retinopathy: Inflammation, Microvasculature Defects and Neurodegeneration [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Diabetic retinopathy is a common complication of diabetes mellitus, which appears in one third of all diabetic patients and is a prominent cause of vision loss.
- Closing excerpt
- New potential therapeutics need to interfere with these diabetic complications even before changes in the retina are diagnosed, to prevent neuronal apoptosis and blindness in patients.
- 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 (183 words)
Diabetic retinopathy is a common complication of diabetes mellitus, which appears in one third of all diabetic patients and is a prominent cause of vision loss. First discovered as a microvascular disease, intensive research in the field identified inflammation and neurodegeneration to be part of diabetic retinopathy. Microglia, the resident monocytes of the retina, are activated due to a complex interplay between the different cell types of the retina and diverse pathological pathways. The trigger for developing diabetic retinopathy is diabetes-induced hyperglycemia, accompanied by leukostasis and vascular leakages. Transcriptional changes in activated microglia, mediated via the nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) and extracellular signal-regulated kinase (ERK) signaling pathways, results in release of various pro-inflammatory mediators, including cytokines, chemokines, caspases and glutamate. Activated microglia additionally increased proliferation and migration. Among other consequences, these changes in microglia severely affected retinal neurons, causing increased apoptosis and subsequent thinning of the nerve fiber layer, resulting in visual loss. New potential therapeutics need to interfere with these diabetic complications even before changes in the retina are diagnosed, to prevent neuronal apoptosis and blindness in patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29301251 · DOI · PMC5796059
Plastic roles of pericytes in the blood-retinal barrier [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The blood-retinal barrier (BRB) consists of tightly interconnected capillary endothelial cells covered with pericytes and glia, but the role of the pericytes in BRB regulation is not fully understood.
- Closing excerpt
- Accordingly, either blocking Ang2 or activating Tie2 greatly attenuates BRB breakdown, suggesting potential therapeutic approaches to reduce retinal damages upon DR progression.
- 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 (156 words)
The blood-retinal barrier (BRB) consists of tightly interconnected capillary endothelial cells covered with pericytes and glia, but the role of the pericytes in BRB regulation is not fully understood. Here, we show that platelet-derived growth factor (PDGF)-B/PDGF receptor beta (PDGFRβ) signalling is critical in formation and maturation of BRB through active recruitment of pericytes onto growing retinal vessels. Impaired pericyte recruitment to the vessels shows multiple vascular hallmarks of diabetic retinopathy (DR) due to BRB disruption. However, PDGF-B/PDGFRβ signalling is expendable for maintaining BRB integrity in adult mice. Although selective pericyte loss in stable adult retinal vessels surprisingly does not cause BRB disintegration, it sensitizes retinal vascular endothelial cells (ECs) to VEGF-A, leading to upregulation of angiopoietin-2 (Ang2) in ECs through FOXO1 activation and triggering a positive feedback that resembles the pathogenesis of DR. Accordingly, either blocking Ang2 or activating Tie2 greatly attenuates BRB breakdown, suggesting potential therapeutic approaches to reduce retinal damages upon DR progression.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28508859 · DOI · PMC5440855
A novel transgenic zebrafish model for blood-brain and blood-retinal barrier development [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundDevelopment and maintenance of the blood-brain and blood-retinal barrier is critical for the homeostasis of brain and retinal tissue.
- Closing excerpt
- The Tg(l-fabp:DBP-EGFP) zebrafish will have great advantages in studying development and maintenance of the blood-neural barrier, which is a new application for the widely used vertebrate model.
- 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 (234 words)
BackgroundDevelopment and maintenance of the blood-brain and blood-retinal barrier is critical for the homeostasis of brain and retinal tissue. Despite decades of research our knowledge of the formation and maintenance of the blood-brain (BBB) and blood-retinal (BRB) barrier is very limited. We have established an in vivo model to study the development and maintenance of these barriers by generating a transgenic zebrafish line that expresses a vitamin D-binding protein fused with enhanced green fluorescent protein (DBP-EGFP) in blood plasma, as an endogenous tracer.ResultsThe temporal establishment of the BBB and BRB was examined using this transgenic line and the results were compared with that obtained by injection of fluorescent dyes into the sinus venosus of embryos at various stages of development. We also examined the expression of claudin-5, a component of tight junctions during the first 4 days of development. We observed that the BBB of zebrafish starts to develop by 3 dpf, with expression of claudin-5 in the central arteries preceding it at 2 dpf. The hyaloid vasculature in the zebrafish retina develops a barrier function at 3 dpf, which endows the zebrafish with unique advantages for studying the BRB.ConclusionZebrafish embryos develop BBB and BRB function simultaneously by 3 dpf, which is regulated by tight junction proteins. The Tg(l-fabp:DBP-EGFP) zebrafish will have great advantages in studying development and maintenance of the blood-neural barrier, which is a new application for the widely used vertebrate model.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 20653957 · DOI · PMC2914679
Chronic dental lighting disrupts blood-retinal barrier homeostasis via vascular and inflammatory pathways [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Excessive lighting is integral to dentists' daily routines but can impair their vision, affecting personal and professional performance.
- Closing excerpt
- This study explored the potential mechanism of dental lighting environment inducing the disruption of blood-retinal barrier homeostasis, and provided essential guidance for dental professionals in selecting light sources, which is conducive to reducing the risk of occupational ocular diseases among dentists.
- 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 (205 words)
Excessive lighting is integral to dentists' daily routines but can impair their vision, affecting personal and professional performance. Most studies focus on acute photodamage, neglecting chronic photo-injury from dental lighting and its impact on the blood-retinal barrier homeostasis. An epidemiological survey involving 14,523 individuals showed dentists had 3.6 times higher odds of vision-related issues compared to other occupations (OR = 3.639, 95% CI: 3.064-4.323). Subsequently, chronic photodamage models in rats were created to accurately simulate dental working conditions. Using systematic imaging and gene analysis, including OCT, tissue clearing technology and RNA-sequencing, dental lighting was found to disrupted both inner and outer blood-retinal barriers, reduced retinal blood vessels, and promoted perivascular macrophage recruitment. Among them, the number of capillary branches decreased sharply. Moreover, the activation of inflammatory-related pathways such as NF-κB signaling resulted in the damage of vision-related functional structures in the retina. Notably, among three dental light sources, low-intensity halogen caused minimal retinal damage, whereas blue and white LEDs significantly disrupted blood-retinal barrier homeostasis. This study explored the potential mechanism of dental lighting environment inducing the disruption of blood-retinal barrier homeostasis, and provided essential guidance for dental professionals in selecting light sources, which is conducive to reducing the risk of occupational ocular diseases among dentists.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41680131 · DOI · PMC12902021
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 Molecular basis of the inner blood-retinal barrier and its breakdown in diabetic macular edema and other pathological conditions [5]
- Research article Current understanding of the molecular and cellular pathology of diabetic retinopathy [6]
- Research article Blood-retinal barrier [7]
- Research article The retinal pigment epithelium: something more than a constituent of the blood-retinal barrier--implications for the pathogenesis of diabetic retinopathy [8]
- Research article Blood-retinal barrier in hypoxic ischaemic conditions: basic concepts, clinical features and management [9]
- Research article The inner blood-retinal barrier: Cellular basis and development [10]
References
- Altmann C, Schmidt MHH. The Role of Microglia in Diabetic Retinopathy: Inflammation, Microvasculature Defects and Neurodegeneration. . 2018. PMID 29301251 · DOI · PMC5796059
- Park DY, Lee J, Kim J, Kim K, Hong S, Han S, et al.. Plastic roles of pericytes in the blood-retinal barrier. . 2017. PMID 28508859 · DOI · PMC5440855
- Xie J, Farage E, Sugimoto M, Anand-Apte B. A novel transgenic zebrafish model for blood-brain and blood-retinal barrier development. . 2010. PMID 20653957 · DOI · PMC2914679
- Sun H, Meng S, Cai H, Xu Z, Gai K, Meng D, et al.. Chronic dental lighting disrupts blood-retinal barrier homeostasis via vascular and inflammatory pathways. . 2026. PMID 41680131 · DOI · PMC12902021
- Klaassen I, Van Noorden CJ, Schlingemann RO. Molecular basis of the inner blood-retinal barrier and its breakdown in diabetic macular edema and other pathological conditions. Prog Retin Eye Res. 2013. PMID 23416119 · DOI
- Antonetti DA, Silva PS, Stitt AW. Current understanding of the molecular and cellular pathology of diabetic retinopathy. Nat Rev Endocrinol. 2021. PMID 33469209 · DOI · PMC9053333
- Cunha-Vaz J, Bernardes R, Lobo C. Blood-retinal barrier. Eur J Ophthalmol. 2011. PMID 23264323 · DOI
- Simó R, Villarroel M, Corraliza L, Hernández C, Garcia-Ramírez M. The retinal pigment epithelium: something more than a constituent of the blood-retinal barrier--implications for the pathogenesis of diabetic retinopathy. J Biomed Biotechnol. 2010. PMID 20182540 · DOI · PMC2825554
- Kaur C, Foulds WS, Ling EA. Blood-retinal barrier in hypoxic ischaemic conditions: basic concepts, clinical features and management. Prog Retin Eye Res. 2008. PMID 18940262 · DOI
- Díaz-Coránguez M, Ramos C, Antonetti DA. The inner blood-retinal barrier: Cellular basis and development. Vision Res. 2017. PMID 28619516 · DOI · PMC5723228
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.