ArticleInvestigative ophthalmology & visual science2026
Degeneration of Interpericyte Tunneling Nanotubes Can Occur in the Absence of Pericyte Loss in Diabetic Retina Disease.
Article in Investigative ophthalmology & visual science, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Interpericyte tunneling nanotubes (IP-TNTs) synchronize pericyte-pericyte communication and regulate microvascular perfusion, processes disrupted in early diabetic retina disease (DRD). We conducted a comprehensive histological examination of IP-TNTs in the normal and diabetic retina using the streptozotocin (STZ)-induced rat model. Methods: High-resolution confocal microscopy was used to assess IP-TNT density, morphology, and their interactions with pericytes and retinal glia. Quantitative analysis was performed on vessel density, capillary diameter, pericyte distribution, and IP-TNT characteristics across three retinal vascular layers: superior vascular plexus (SVP), intermediate capillary plexus, and deep capillary plexus (DCP). Results: IP-TNTs were present across all retinal vascular plexuses, with the highest density in the SVP and DCP. Diabetic retinas exhibited a significant reduction in IP-TNT density, length, and morphological diversity, particularly in the DCP. The loss of IP-TNTs occurred independently of capillary loss and was associated with preserved vessel density and increased pericyte numbers. Notably, there was a shift in IP-TNT phenotype, with a significant increase in Type 1 (soma-to-soma) IP-TNTs in the DCP of diabetic rats. IP-TNTs were closely associated with retinal glial cells, including astrocytes and Müller cells, suggesting a role in neurovascular-glial interactions. Conclusion: Our findings indicate that IP-TNTs are critical components of the retinal microvascular network, and their early degeneration in diabetes may contribute to impaired microvascular autoregulation and pericyte dysfunction. The selective loss of IP-TNTs in the DCP highlights their potential as early biomarkers of diabetic microvascular injury. Modulating IP-TNT stability may represent a promising strategy for early intervention in diabetic retinopathy.
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.