Evidence map›Paper›PMID 40079201›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025

Retinoid X receptor agonist 9CDHRA mitigates retinal ganglion cell apoptosis and neuroinflammation in a mouse model of glaucoma.

Devaraj Basavarajappa, Nitin Chitranshi, Seyed Shahab Oddin Mirshahvaladi, Veer B Gupta, Viswanthram Palanivel, Gabriella E Parrilla, Akanksha Salkar, Mehdi Mirzaei, András M Komáromy, Wojciech Krezel and 2 more

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. 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. Article
  2. Review
  3. Retinoid X receptor agonist 9CDHRA mitigates retinal ganglion cell apoptosis and neuroinflammation in a mouse model of glaucoma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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

12 authors.

Devaraj BasavarajappaMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia.ORCID https://orcid.org/0000-0003-0997-0196
Nitin ChitranshiMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia.ORCID https://orcid.org/0000-0002-6508-9865
Seyed Shahab Oddin MirshahvaladiMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia.ORCID https://orcid.org/0000-0002-9145-6155
Veer B GuptaSchool of Medicine, Deakin University, Geelong, Victoria, Australia.ORCID https://orcid.org/0000-0003-4989-0764
Viswanthram PalanivelMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia.ORCID https://orcid.org/0000-0002-4649-5913
Gabriella E ParrillaMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia.ORCID https://orcid.org/0009-0001-2991-0310
Akanksha SalkarMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia.ORCID https://orcid.org/0000-0001-9941-0947
Mehdi MirzaeiMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia.ORCID https://orcid.org/0000-0001-8727-4984
András M KomáromyDepartment of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan, USA.ORCID https://orcid.org/0000-0002-8845-0588
Wojciech KrezelInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Institut de la Santé et de la Recherche Médicale (U1258), Centre National de la Recherche Scientifique (UMR7104), Université de Strasbourg, Fédération de Médecine Translationnelle de Strasbourg, Illkirch, France.ORCID https://orcid.org/0000-0003-1605-3185
Stuart L GrahamMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia.ORCID https://orcid.org/0000-0001-7519-969X
Vivek GuptaMacquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia.ORCID https://orcid.org/0000-0002-0202-7843

Funding

Australian Vision Research (AVR)DHAC | National Health and Medical Research Council (NHMRC)
6 · The paper itself

Abstract

Glaucoma, a leading cause of irreversible blindness, is characterized by the progressive loss of retinal ganglion cells (RGCs) and optic nerve damage, often associated with elevated intraocular pressure (IOP). Retinoid X receptors (RXRs) are ligand-activated transcription factors crucial for neuroprotection, as they regulate gene expression to promote neuronal survival via several biochemical networks and reduce neuroinflammation. This study investigated the therapeutic potential of 9-cis-13,14-dihydroretinoic acid (9CDHRA), an endogenous retinoid RXR agonist, in mitigating RGC degeneration in a high-IOP-induced experimental model of glaucoma. We administered 9CDHRA to glaucomatous mice eyes via intravitreal injections and assessed its effects on endoplasmic reticulum (ER) stress markers, glial cell activation, and RGC survival. Our findings demonstrated that 9CDHRA treatment significantly protected inner retinal function and retinal laminar structure in high-IOP glaucoma. The treatment reduced ER stress markers, increased protein lysine acetylation, and diminished glial cell activation, leading to a significant decrease in apoptotic cells under glaucomatous conditions. These results suggest that 9CDHRA exerts neuroprotective effects by modulating key pathogenic pathways in glaucoma, highlighting its potential as a novel therapeutic strategy for preserving vision in glaucoma.

Indexed as

ApoptosisGlaucomaNeuroinflammatory DiseasesRetinal Ganglion CellsRetinoid X ReceptorsTretinoinAnimalsDisease Models, AnimalEndoplasmic Reticulum StressIntraocular PressureMaleMiceMice, Inbred C57BLNeuroprotective AgentsNeuroprotective AgentsRetinoid X ReceptorsTretinoin9CDHRAapoptosisER stressglaucomaglial cellintraocular pressureneuroinflammationneuroprotectionretinoid X receptors

Identifiers

PMID40079201
PMCPMC11904862

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.