ReviewFrontiers in endocrinology2026
Neurovascular unit uncoupling in diabetic retinopathy: molecular mechanisms and stage-adapted therapeutic strategies.
Review in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic retinopathy (DR) is a major neurovascular complication of diabetes and remains a leading cause of vision loss among working-age adults worldwide. Although DR has traditionally been classified as a microvascular complication, it is now increasingly recognized as a neurovascular degenerative disorder involving coordinated injury to neuronal, glial, vascular, and extracellular matrix components of the retinal neurovascular unit (NVU). The NVU provides the structural and functional basis for coupling neuronal activity to local blood flow and for maintaining retinal immune and barrier homeostasis. In diabetes, chronic hyperglycemia, oxidative stress, inflammation, metabolic dysregulation, impaired vascular endothelial growth factor (VEGF)/angiopoietin-Tie (Ang/Tie) signaling, abnormal intercellular communication, and epigenetic memory progressively disrupt the coordinated interactions among NVU components, leading to neurovascular uncoupling. This concept helps explain why retinal functional abnormalities and neurodegenerative changes may precede clinically visible vascular lesions. In this review, we summarize cell-specific NVU alterations and the molecular mechanisms that drive neurovascular uncoupling in DR. We also discuss how this framework may support earlier diagnosis, mechanism-based phenotyping, and stage-adapted treatment strategies. Established therapies, including anti-vascular endothelial growth factor (anti-VEGF) agents, corticosteroids, and angiopoietin-2 (Ang-2)/Tie-2-directed vascular stabilization, are considered together with investigational approaches targeting oxidative stress, inflammation, neuroprotection, metabolic reprogramming, epigenetic regulation, and drug delivery. Reframing DR as a diabetes-driven disorder of early NVU uncoupling may help shift clinical thinking from late vascular rescue toward mechanism-based neurovascular protection, precision phenotyping, and stage-adapted intervention.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.