Evidence map›Paper›PMID 41635083›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2026

CaMKII-based gene therapy protects retinal ganglion cells in a broad range of disease: ischemic retinopathy and congenital glaucoma.

Jing Zhou, Yue Wan, Michael G Anderson, Elia J Duh, Jonathan B Demb, Xinzheng Guo, Bo Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
–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

1 citing paper in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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

7 authors.

Jing ZhouEye Research Institute, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China; Department of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Yue WanState Key Laboratory of Common Mechanism Research for Major Diseases, Suzhou Institute of Systems Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Suzhou, Jiangsu 215123, China; Department of Ophthalmology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
Michael G AndersonDepartment of Molecular Physiology and Biophysics, University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA.
Elia J DuhDepartment of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Jonathan B DembDepartment of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, CT 06511, USA; Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06511, USA; Department of Neuroscience, Yale University School of Medicine, New Haven, CT 06511, USA.
Xinzheng GuoState Key Laboratory of Common Mechanism Research for Major Diseases, Suzhou Institute of Systems Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Suzhou, Jiangsu 215123, China. Electronic address: gxz@ism.pumc.edu.cn.
Bo ChenEye Research Institute, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China; Department of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Electronic address: bochen@scu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Degeneration of retinal ganglion cells (RGCs) and their axons, as observed in ischemic retinopathy and glaucoma, results in irreversible vision loss. Elevated intraocular pressure (IOP) is a key factor driving these conditions, with existing treatments focused on IOP reduction often proving inadequate to halt disease progression. Here, we report that CaMKII-based gene therapy robustly protects RGCs and preserves visual function in mouse models of ischemic injury and congenital glaucoma, positioning CaMKII as a broad therapeutic target for retinal diseases driven by acute and chronic IOP elevation that damage RGCs.

Indexed as

Calcium-Calmodulin-Dependent Protein Kinase Type 2Genetic TherapyGlaucomaIschemiaRetinal DiseasesRetinal Ganglion CellsAnimalsDisease Models, AnimalGene Therapy AgentsGenetic VectorsHumansIntraocular PressureMiceCalcium-Calmodulin-Dependent Protein Kinase Type 2CaMKII-based gene therapycongenital glaucomaischemic retinopathyneuroprotectionretinal ganglion cellsvision preservation

Identifiers

PMID41635083
PMCPMC13154303

What OpenQuestion holds

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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.