Evidence map›Paper›PMID 41102382›Full record

ArticleCommunications biology2025

OPTN protects retinal ganglion cells and ameliorates neuroinflammation in optic neuropathies.

Qinglong Wang, Yiqi Wang, Yi Da Douglas Jiang, Ryan Donahue, Gaby Cao, Weixuan Yan, Hong Guo, Zhenghui Li, Jenna Liang, Jin Hao and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. 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

14 authors.

Qinglong Wang *Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-3074-4786
Yiqi Wang *Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Yi Da Douglas JiangDepartment of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Ryan DonahueF.M. Kirby Neurobiology Center, Boston Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA, USA.
Gaby CaoDepartment of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Weixuan YanDepartment of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Hong GuoDepartment of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Zhenghui LiDepartment of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Jenna LiangDepartment of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Jin HaoDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.ORCID http://orcid.org/0000-0002-6685-2017
Yi LuDepartment of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Fengfeng BeiDepartment of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Qianbin WangDepartment of Biomedical Engineering, Binghamton University, State University of New York, Binghamton, NY, USA.ORCID http://orcid.org/0000-0002-9840-6732
Feng TianDepartment of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. ftian@bidmc.harvard.edu.ORCID http://orcid.org/0000-0001-8965-8973

Funding

Epigenomic mechanisms regulating RGC survival and axon regenerationR00EY032181 · NEI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Feng Tian · 2024 to 2026
$750k
Epigenomic mechanisms regulating RGC survival and axon regenerationK99EY032181 · NEI · BOSTON CHILDREN'S HOSPITAL · PI TIAN, FENG · 2021 to 2023
$282k
NEI NIH HHS K99 EY032181NEI NIH HHS R00 EY032181U.S. Department of Health & Human Services | NIH | National Eye Institute (NEI) EY032181
6 · The paper itself

Abstract

Optineurin (OPTN) is an adaptor protein that plays a crucial role in many cellular pathways, including NF-κB signaling, programmed cell death, and vesicular trafficking. OPTN dysfunction has been implicated in the pathogenesis of several diseases, such as primary open angle glaucoma (POAG), amyotrophic lateral sclerosis (ALS). While mutations of OPTN seem to be predominantly loss-of-function in ALS, only gain-of-function mechanisms have been reported in POAG. Here, we demonstrate that OPTN knockout in the retina contributes to short-term astrogliosis, retinal ganglion cell (RGC) loss and long-term microglial activation. Moreover, OPTN loss of function does not exacerbate RGC death induced by ocular hypertension. Integrated bioinformatics and immunofluorescence analyses reveal that OPTN dysfunction leads to neuropeptide Y (NPY) downregulation and CHOP upregulation. Overexpression of wild-type OPTN in a hypertension glaucoma model prevents the RGC loss and attenuates microglial activation. Together, our findings highlight a neuroprotective role for OPTN as a key neuroimmune modulator.

Indexed as

Cell Cycle ProteinsMembrane Transport ProteinsNeuroinflammatory DiseasesOptic Nerve DiseasesRetinal Ganglion CellsTranscription Factor TFIIIAAnimalsDisease Models, AnimalGlaucomaHumansMaleMiceMice, Inbred C57BLMice, KnockoutCell Cycle ProteinsMembrane Transport ProteinsOptn protein, mouseTranscription Factor TFIIIA

Identifiers

PMID41102382
PMCPMC12533019

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.