Evidence map›Paper›PMID 30233053›Full record

ReviewNeural regeneration research2018

The unfolded protein response signaling and retinal Müller cell metabolism.

Kristen Kelly, Joshua J Wang, Sarah X Zhang

Open access · goldAbstract readReview
In one paragraph

Review in Neural regeneration research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Neuroprotection in Diabetes Retinal Disease: An Unmet Medical Need.International journal of molecular sciences · 2026
    Review
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  11. Targeted Blood Metabolomic Study on Retinopathy of Prematurity.Investigative ophthalmology & visual science · 2020
    Article
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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.

Kristen KellyDepartment of Ophthalmology and Neuroscience Program, Ross Eye Institute, University at Buffalo, State University of New York, Buffalo, NY, USA.
Joshua J WangDepartment of Ophthalmology and Neuroscience Program, Ross Eye Institute, University at Buffalo; SUNY Eye Institute, State University of New York, Buffalo, NY, USA.
Sarah X ZhangDepartment of Ophthalmology and Neuroscience Program, Ross Eye Institute, University at Buffalo; SUNY Eye Institute, State University of New York, Buffalo, NY, USA.
University at Buffalo, State University of New York · US

Funding

ER Stress and Diabetic RetinopathyR01EY019949 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZHANG, SARAH X · 2010 to 2023
$5.5M
Study of the ER-mitochondria interface as a new target in diabetic retinopathyR21EY025061 · NEI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI ZHANG, SARAH X · 2015 to 2016
$438k
NEI NIH HHS R01 EY019949NEI NIH HHS R21 EY025061
6 · The paper itself

Abstract

The retina is one of the most energy demanding tissues in the body. Like most neurons in the central nervous system, retinal neurons consume high amounts of adenosine-5'-triphosphate (ATP) to generate visual signal and transmit the information to the brain. Disruptions in retinal metabolism can cause neuronal dysfunction and degeneration resulting in severe visual impairment and even blindness. The homeostasis of retinal metabolism is tightly controlled by multiple signaling pathways, such as the unfolded protein response (UPR), and the close interactions between retinal neurons and other retinal cell types including vascular cells and Müller glia. The UPR is a highly conserved adaptive cellular response and can be triggered by many physiological stressors and pathophysiological conditions. Activation of the UPR leads to changes in glycolytic rate, ATP production, de novo serine synthesis, and the hexosamine biosynthetic pathway, which are considered critical components of Müller glia metabolism and provide metabolic support to surrounding neurons. When these pathways are disrupted, neurodegeneration occurs rapidly. In this review, we summarize recent advance in studies of the UPR in Müller glia and highlight the potential role of the UPR in retinal degeneration through regulation of Müller glia metabolism.

Indexed as

glucose transporterglycolysismetabolismMüller glianeurodegenerationretinaunfolded protein responseX-box binding protein 1

Identifiers

PMID30233053
PMCPMC6183030
OpenAlexW2890292041

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.