Evidence map›Paper›PMID 28674171›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017

Vascular Pericyte Impairment and Connexin43 Gap Junction Deficit Contribute to Vasomotor Decline in Diabetic Retinopathy.

Elena Ivanova, Tamas Kovacs-Oller, Botir T Sagdullaev

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
4.3field-weighted citation impact, top 5% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 88 citations in OpenAlex.

  1. Skin capillary endothelial cells form a network of spatiotemporally conserved CaProceedings of the National Academy of Sciences of the United States of America · 2026
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  6. Associations of retinal neurovascular dysfunction with inner retinal layer thickness in non-proliferative diabetic retinopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2024
    Article
  7. Cells · 2024
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  8. Article
  9. Article
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  11. Article
  12. Therapeutic Potential of Fingolimod in Diabetes Mellitus and Its Chronic Complications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Connexins Biology in the Pathophysiology of Retinal Diseases.Advances in experimental medicine and biology · 2023
    Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Elena IvanovaDepartment of Ophthalmology, Brain and Mind Research Institute, Weill Cornell Medicine, Burke Medical Research Institute, White Plains, New York 10605.
Tamas Kovacs-OllerDepartment of Ophthalmology, Brain and Mind Research Institute, Weill Cornell Medicine, Burke Medical Research Institute, White Plains, New York 10605.
Botir T SagdullaevDepartment of Ophthalmology, Brain and Mind Research Institute, Weill Cornell Medicine, Burke Medical Research Institute, White Plains, New York 10605 bos2005@med.cornell.edu.ORCID 0000-0002-0611-1479
Cornell University · US

Funding

Vascular control in diabetic retinopathyR01EY026576 · NEI · WINIFRED MASTERSON BURKE MED RES INST · PI SAGDULLAEV, BOTIR T. · 2016 to 2020
$2.9M
NEI NIH HHS R01 EY026576
6 · The paper itself

Abstract

Adequate blood flow is essential to brain function, and its disruption is an early indicator in diseases, such as stroke and diabetes. However, the mechanisms contributing to this impairment remain unclear. To address this gap, in the diabetic and nondiabetic male mouse retina, we combined an unbiased longitudinal assessment of vasomotor activity along a genetically defined vascular network with pharmacological and immunohistochemical analyses of pericytes, the capillary vasomotor elements. In nondiabetic retina, focal stimulation of a pericyte produced a robust vasomotor response, which propagated along the blood vessel with increasing stimulus. In contrast, the magnitude, dynamic range, a measure of fine vascular diameter control, and propagation of vasomotor response were diminished in diabetic retinas from streptozotocin-treated mice. These functional changes were linked to several mechanisms. We found that density of pericytes and their sensitivity to stimulation were reduced in diabetes. The impaired response propagation from the stimulation site was associated with lower expression of connexin43, a major known gap junction unit in vascular cells. Indeed, selective block of gap junctions significantly reduced propagation but not initiation of vasomotor response in the nondiabetic retina. Our data establish the mechanisms for fine local regulation of capillary diameter by pericytes and a role for gap junctions in vascular network interactions. We show how disruption of this balance contributes to impaired vasomotor control in diabetes.

Indexed as

AnimalsBlood Flow VelocityConnexin 43Diabetes Mellitus, ExperimentalDiabetic RetinopathyGap JunctionsMaleMiceMice, Inbred C57BLPericytesRetinal VesselsConnexin 43connexin43diabetesdiabetic retinopathyfunctional hyperemiapericyte

Identifiers

PMID28674171
PMCPMC5551058
OpenAlexW2727380805

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.