Evidence map›Paper›PMID 34297923›Full record

ArticleCell2021

Preservation of vision after CaMKII-mediated protection of retinal ganglion cells.

Xinzheng Guo, Jing Zhou, Christopher Starr, Ethan J Mohns, Yidong Li, Earnest P Chen, Yonejung Yoon, Christopher P Kellner, Kohichi Tanaka, Hongbing Wang and 5 more

Open access · greenAbstract read
In one paragraph

Article in Cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 2 pooled it
10.1field-weighted citation impact, top 1% of its field
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

106 citing papers in PubMed, 2 syntheses or guidelines pooled it, 172 citations in OpenAlex.

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46 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 2 countries.

Xinzheng GuoDepartment of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Jing ZhouDepartment of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Christopher StarrDepartment of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Ethan J MohnsDepartment of Neuroscience, Yale University School of Medicine, New Haven, CT 06511, USA.
Yidong LiDepartment of Neuroscience, Yale University School of Medicine, New Haven, CT 06511, USA.
Earnest P ChenYale College, New Haven, CT 06520, USA.
Yonejung YoonDepartment of Neurosurgery, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Christopher P KellnerDepartment of Neurosurgery, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Kohichi TanakaLaboratory of Molecular Neuroscience, School of Biomedical Sciences and Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Hongbing WangDepartment of Physiology, Michigan State University, East Lansing, MI 48824, USA.
Wei LiuDepartment of Ophthalmology and Visual Sciences, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Louis R PasqualeDepartment of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Jonathan B DembDepartment of Neuroscience, Yale University School of Medicine, New Haven, CT 06511, USA; Department 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.
Michael C CrairDepartment of Neuroscience, Yale University School of Medicine, New Haven, CT 06511, USA; Department of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, CT 06511, USA.
Bo ChenDepartment of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Electronic address: bo.chen@mssm.edu.
Icahn School of Medicine at Mount Sinai · USYale University · USAlbert Einstein College of Medicine · USMichigan State University · USTokyo Medical and Dental University · JP

Funding

Mechanisms of Visual Map Development in the Thalamus and Superior ColliculusR01EY015788 · NEI · YALE UNIVERSITY · PI Michael C. Crair · 2005 to 2026
$7.9M
Yale Core Grant for Vision ResearchP30EY026878 · NEI · YALE UNIVERSITY · PI In-Jung Kim · 2016 to 2026
$7.1M
Neural Circuits and Synapses for Early Visual ProcessingR01EY014454 · NEI · YALE UNIVERSITY · PI DEMB, JONATHAN B · 2005 to 2022
$6.7M
Gene regulation of retinal cell differentiationR01EY022645 · NEI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI WEI LIU · 2013 to 2026
$4.6M
CaMKII-mediated Neuroprotection of Retinal Ganglion CellsR01EY028921 · NEI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CHEN, BO · 2019 to 2022
$2.4M
Mechanism underlying cognitive and synaptic flexibilityR01MH124992 · NIMH · MICHIGAN STATE UNIVERSITY · PI WANG, HONGBING · 2021 to 2024
$2.0M
Regeneration of rod photoreceptors from Muller glial cells in adult mouse retinaR01EY024986 · NEI · YALE UNIVERSITY · PI CHEN, BO · 2016 to 2019
$1.6M
Modeling CRB1-related retinal disease using 3-D human retinal organoidsR21EY029806 · NEI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI LIU, WEI · 2019 to 2020
$461k
NEI NIH HHS P30 EY026878NEI NIH HHS R01 EY014454NEI NIH HHS R01 EY015788NEI NIH HHS R01 EY022645NEI NIH HHS R01 EY024986NEI NIH HHS R01 EY028921NEI NIH HHS R21 EY029806NIMH NIH HHS R01 MH124992
6 · The paper itself

Abstract

Retinal ganglion cells (RGCs) are the sole output neurons that transmit visual information from the retina to the brain. Diverse insults and pathological states cause degeneration of RGC somas and axons leading to irreversible vision loss. A fundamental question is whether manipulation of a key regulator of RGC survival can protect RGCs from diverse insults and pathological states, and ultimately preserve vision. Here, we report that CaMKII-CREB signaling is compromised after excitotoxic injury to RGC somas or optic nerve injury to RGC axons, and reactivation of this pathway robustly protects RGCs from both injuries. CaMKII activity also promotes RGC survival in the normal retina. Further, reactivation of CaMKII protects RGCs in two glaucoma models where RGCs degenerate from elevated intraocular pressure or genetic deficiency. Last, CaMKII reactivation protects long-distance RGC axon projections in vivo and preserves visual function, from the retina to the visual cortex, and visually guided behavior.

Indexed as

CytoprotectionVision, OcularAnimalsAxonsBrainCalcium-Calmodulin-Dependent Protein Kinase Type 2Cyclic AMP Response Element-Binding ProteinDependovirusDisease Models, AnimalEnzyme ActivationGlaucomaMiceMice, Inbred C57BLNeurotoxinsOptic Nerve InjuriesRetinal Ganglion CellsCalcium-Calmodulin-Dependent Protein Kinase Type 2Cyclic AMP Response Element-Binding ProteinNeurotoxinsCaMKIICREBexcitotoxicityglaucomaoptic nerve crushRGCRGC protectionvision preservationvisual functionvisual pathway

Identifiers

PMID34297923
PMCPMC8530265
OpenAlexW3187045755

What OpenQuestion holds

Textmetadata
LicenceTDM
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.