Evidence map›Paper›PMID 42320266›Full record

ArticleRedox biology2026

Redox imbalance dictates dependence on GOT1 versus GOT2 for rod photoreceptor health during aging and stress.

Meini Chen, Eric Weh, Moloy T Goswami, Katherine M Weh, Heather Hager, Peter Sajjakulnukit, Avi J Weingarten, Shubha Subramanya, Nicholas Miller, Sraboni Chaudhury and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Meini ChenDepartment of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI, United States; Eye Center of Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Eric WehDepartment of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI, United States.
Moloy T GoswamiDepartment of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI, United States.
Katherine M WehDepartment of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI, United States.
Heather HagerDepartment of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI, United States.
Peter SajjakulnukitDepartment of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI, United States.
Avi J WeingartenDepartment of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI, United States.
Shubha SubramanyaDepartment of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI, United States.
Nicholas MillerDepartment of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI, United States.
Sraboni ChaudhuryDepartment of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI, United States.
Emma PirainoDepartment of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI, United States.
Navdeep S ChandelDepartment of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, IL, United States; Department of Medicine, Division of Pulmonary and Critical Care, Northwestern University Feinberg School of Medicine, Chicago, IL, United States.
Renee C RyalsDepartment of Ophthalmology, Casey Eye Institute, Oregon Health & Science University, Portland, OR, United States.
Costas A LyssiotisDepartment of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI, United States; Department of Internal Medicine, Division of Gastroenterology and Hepatology, University of Michigan, Ann Arbor, MI, United States; Rogel Cancer Center, University of Michigan, Ann Arbor, MI, United States.
Thomas J WubbenDepartment of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI, United States. Electronic address: twubben@med.umich.edu.

Funding

VIVARIUM MODULEP30EY007003 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI David Antonetti · 1987 to 2026
$17.6M
NEI NIH HHS P30 EY007003
6 · The paper itself

Abstract

Photoreceptor (PR) loss causes vision loss in many blinding diseases and effective therapies to prevent this cell loss are lacking. Aspartate aminotransferases (GOTs), located in the cytosol (GOT1) and mitochondria (GOT2), are key components of the malate-aspartate shuttle, which transfers reducing equivalents from cytosol to mitochondria. Previous work has implicated the GOTs as potential modulators of blinding retinal disease. To determine the roles of GOT1 and GOT2 in rod PRs, we generated rod PR-specific Got1 or Got2 conditional knockout mice (Got1 or Got2 cKO). We previously showed that Got1 cKO causes PR degeneration and is accompanied by NADH accumulation and a decreased retinal NAD

Indexed as

AgingRetinal Rod Photoreceptor CellsStress, PhysiologicalAnimalsMiceMice, KnockoutMitochondriaNADNicotinamide-Nucleotide AdenylyltransferaseOxidation-ReductionOxidative StressRetinal DegenerationNADNicotinamide-Nucleotide AdenylyltransferaseNmnat1 protein, mouseGOT1GOT2MetabolismNeuroprotectionPhotoreceptor

Identifiers

PMID42320266
PMCPMC13315887

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.