Evidence map›Paper›PMID 38824526›Full record

ArticleJournal of neuroinflammation2024

cFLIP in the molecular regulation of astroglia-driven neuroinflammation in experimental glaucoma.

Xiangjun Yang, Qun Zeng, Maide Gözde İnam, Onur İnam, Chyuan-Sheng Lin, Gülgün Tezel

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

6 authors.

Xiangjun YangDepartment of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA.
Qun ZengDepartment of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA.
Maide Gözde İnamDepartment of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA.
Onur İnamDepartment of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA.
Chyuan-Sheng LinDepartment of Pathology & Cell Biology, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA.
Gülgün TezelDepartment of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA. gt2320@cumc.columbia.edu.

Funding

Tumor Biology and Microenvironment ProgramP30CA013696 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Anil K Rustgi · 1985 to 2026
$115.3M
Instrumentation, Fabrication, and Design CoreP30EY019007 · NEI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Xin Zhang · 2010 to 2026
$12.9M
Modulation of Neuroinflammation in GlaucomaR01EY033359 · NEI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TEZEL, GULGUN · 2022 to 2025
$1.6M
NCI NIH HHS P30 CA013696NEI NIH HHS P30 EY019007NEI NIH HHS R01 EY033359NEI NIH HHS R01 EY033359, P30 EY019007NIH HHS P30 CA013696Research to Prevent Blindness Departmental Core Grant
6 · The paper itself

Abstract

backgroundRecent experimental studies of neuroinflammation in glaucoma pointed to cFLIP as a molecular switch for cell fate decisions, mainly regulating cell type-specific caspase-8 functions in cell death and inflammation. This study aimed to determine the importance of cFLIP for regulating astroglia-driven neuroinflammation in experimental glaucoma by analyzing the outcomes of astroglia-targeted transgenic deletion of cFLIP or cFLIP

methodsGlaucoma was modeled by anterior chamber microbead injections to induce ocular hypertension in mouse lines with or without conditional deletion of cFLIP or cFLIP

resultsImmunoassays and immunolabeling of retina and optic nerve tissues presented reduced production of various proinflammatory cytokines, including TNFα, in GFAP/cFLIP and GFAP/cFLIP

conclusionsA prominent response limiting neuroinflammation in ocular hypertensive eyes with cFLIP-deletion in astroglia values the role of cFLIP in the molecular regulation of glia-driven neuroinflammation during glaucomatous neurodegeneration. The molecular responses accompanying the lessening of neurodegenerative inflammation also seem to maintain astroglia survival despite increased caspase-8 cleavage with cFLIP deletion. A transcriptional autoregulatory response, dampening RelA but boosting RelB for selective expression of NF-κB target genes, might reinforce cell survival in cFLIP-deleted astroglia.

Indexed as

AstrocytesCASP8 and FADD-Like Apoptosis Regulating ProteinGlaucomaNeuroinflammatory DiseasesAnimalsCytokinesDisease Models, AnimalGlial Fibrillary Acidic ProteinMiceMice, Inbred C57BLMice, TransgenicOptic NerveRetinaCASP8 and FADD-Like Apoptosis Regulating ProteinCflar protein, mouseCytokinesGlial Fibrillary Acidic ProteinAstrogliacFLIPCytokineGlaucomaNeuroinflammation

Identifiers

PMID38824526
PMCPMC11143607

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Registered trials

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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.