Evidence map›Paper›PMID 40457155›Full record

ArticleNeuroscience bulletin2025

HOCPCA Exerts Neuroprotection on Retinal Ganglion Cells by Binding to CaMKIIα and Modulating Oxidative Stress and Neuroinflammation in Experimental Glaucoma.

Panpan Li, Xin Shi, Hanhan Liu, Yuan Feng, Xiaosha Wang, Marc Herb, Haichao Ji, Stefan Wagner, Johannes Vogt, Verena Prokosch

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience bulletin, 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. 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

10 authors.

Panpan Li *Department of Ophthalmology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, 50937, Germany.
Xin Shi *Department of Ophthalmology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, 50937, Germany.
Hanhan LiuDepartment of Ophthalmology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, 50937, Germany.
Yuan FengDepartment of Ophthalmology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, 50937, Germany.
Xiaosha WangDepartment of Ophthalmology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, 50937, Germany.
Marc HerbInstitute for Medical Microbiology, Immunology and Hygiene, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, 50935, Germany.
Haichao JiMolecular and Translational Neurosciences, CECAD Cluster of Excellence, CMMC Center of Molecular Medicine Cologne, University of Cologne, Cologne, 50931, Germany.
Stefan WagnerMolecular and Translational Neurosciences, CECAD Cluster of Excellence, CMMC Center of Molecular Medicine Cologne, University of Cologne, Cologne, 50931, Germany.
Johannes VogtMolecular and Translational Neurosciences, CECAD Cluster of Excellence, CMMC Center of Molecular Medicine Cologne, University of Cologne, Cologne, 50931, Germany.
Verena ProkoschDepartment of Ophthalmology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, 50937, Germany. verena.prokosch@uk-koeln.de.ORCID http://orcid.org/0000-0002-5318-0637

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal injury in glaucoma persists despite effective intraocular pressure (IOP) control, necessitating neuroprotective strategies for retinal ganglion cells (RGCs). In this study, we investigated the neuroprotective role of the γ-hydroxybutyrate analog HOCPCA in a glaucoma model, focusing on its effects on CaMKII signaling, oxidative stress, and neuroinflammatory responses. Retinal tissue from high IOP animal models was analyzed via proteomics. In vitro mouse retinal explants were subjected to elevated pressure and oxidative stress, followed by HOCPCA treatment. HOCPCA significantly mitigated the RGC loss induced by oxidative stress and elevated pressure, preserving neuronal function. It restored CaMKIIα and β levels, preserving RGC integrity, while also modulating oxidative stress and neuroinflammatory responses. These findings suggest that HOCPCA, through its interaction with CaMKII, holds promise as a neuroprotective therapy for glaucoma.

Indexed as

Calcium-Calmodulin-Dependent Protein Kinase Type 2GlaucomaNeuroinflammatory DiseasesNeuroprotective AgentsOxidative StressRetinal Ganglion CellsAnimalsDisease Models, AnimalIntraocular PressureMaleMiceMice, Inbred C57BLNeuroprotectionCalcium-Calmodulin-Dependent Protein Kinase Type 2Neuroprotective AgentsCaMKIIGlaucomaHOCPCANeuroprotectionRGCs

Identifiers

PMID40457155
PMCPMC12314278

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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.