ReviewInflammopharmacology2025
Targeting the gut-retina axis: mechanistic insights and therapeutic prospects for diabetic retinopathy.
Review in Inflammopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The relationship between diabetic retinopathy and intestinal microbiota: a systematic review and meta analysis.International ophthalmology · 2026Pooled it
- The gut-retina axis in diabetic retinopathy: a new paradigm for pathogenesis and therapeutic intervention.Frontiers in immunology · 2026Review
- Anti-diabetic retinopathy molecular mechanism of Dihuang Yinzi: insights from network pharmacology, metabolomics, and microbiome analysis.Frontiers in medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
The pathogenesis of diabetic retinopathy DR is highly complex, and in recent years, increasing attention has been directed toward the role of the gut in its development. Evidence suggests that intestinal barrier dysfunction is a frequent pathological feature in both DR patients and animal models, facilitating the translocation of gut microbiota and their metabolites into the systemic circulation. On one hand, these translocated microbial components and metabolites activate intestinal immune cells, promoting the migration of gut-derived immune cells to the retina or choroid, thereby contributing to retinal neuroinflammation. On the other hand, they may compromise the integrity of the blood-retina barrier, disrupting the retinal microenvironment. This review explores the influence of the gut on DR pathogenesis through several key mechanisms: alterations in gut microbiota and their metabolites, impairment of intestinal barrier integrity, dysregulated gut immune responses, translocation routes of gut-derived components (including immune cells, microbes, and metabolites) to the retina, and the resulting retinal pathology and microglial-mediated neuroinflammation. By elucidating the pathological mechanisms underlying the gut-retina axis, we aim to identify critical molecular and cellular targets involved in DR progression and to provide new insights for the development of innovative therapeutic strategies.
Indexed as
Identifiers
41207927What 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.