Loss of Kv8.2 in the Mouse Retina Is Associated With Altered One-Carbon Metabolism.

Overview

1. Department of Ophthalmology and Visual Sciences Carver College of Medicine, University of Iowa Iowa Iowa USA
2. Department of Biochemistry and Molecular Biology, Carver College of Medicine University of Iowa Iowa Iowa USA

Abstract

Photoreceptors are highly energy‐demanding neurons, and disruption of photoreceptor signaling remodels retinal metabolism and contributes to degeneration, yet the pathways underlying these changes remain incompletely defined. Kv8.2 knockout (KO) mice, a model of KCNV2 retinopathy, exhibit impaired photoreceptor ion homeostasis and slow rod degeneration, providing an opportunity to investigate metabolic adaptation during progressive dysfunction. Untargeted metabolomic profiling was performed on retinas from wildtype (WT) and Kv8.2 KO mice at 1 and 13 months of age. Principal component analysis revealed distinct profiles for aged Kv8.2 KO retinas compared with aged WT and young groups, while young WT and KO retinas were metabolically similar. The major changes in aged Kv8.2 KO retinas compared to aged WT were reduced nucleobases and nucleosides while the amino acids homocysteine, methionine, and serine were elevated. These are signature metabolites in one‐carbon metabolism, a metabolic hub influencing nucleotide metabolism, epigenic regulation, and anti‐oxidant defense. Supervised modeling showed that these one‐carbon–related changes emerge early and progress with age in Kv8.2 KO retinas. Together, these findings implicate altered one‐carbon metabolism as a key mechanism in photoreceptor vulnerability and adaptation in slow retinal degeneration.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

The paper says that its authors' code is available on request: it was not published with the paper, so there is nothing to verify.

The paper's code and data availability statement is in the Data section.

Tracing map

A tracing map links a paper to the code its authors published: this paper has none (its code is available on request), so it has no map.

Data

No dataset and no data link were found in the paper.

Data Availability Statement

The normalized metabolite amounts are provided in File S1 and the R code used for sPLS‐DA modeling is available on request.

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 2, 28 September 2026

• Publisher: n/a → Wiley

Version 1, 28 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 2 authors, 7 MeSH terms, 2 funders, 59 references.

Cite

This paper

Kruth, K., & Baker, S. A. (2026). Loss of Kv8.2 in the Mouse Retina Is Associated With Altered One-Carbon Metabolism. Journal of neurochemistry, 170(4), e70420. https://doi.org/10.1111/jnc.70420

Similar papers

The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.

[1] doi:10.1016/j.neurobiolaging.2026.04.007 [code]

The TREM2 R47H variant is associated with liver-plasma-brain axis dyshomeostasis in the 5xFAD mouse model of Alzheimer's disease.

Journal: Neurobiology of aging

In common: mouse, cellular / molecular, 2 references

[2] doi:10.1002/imt2.70163 [code]

Spatial multi-omics unveils sphingolipid metabolic reprogramming within the retinal pathological niche.

Journal: iMeta

In common: mouse, cellular / molecular, 1 reference

[3] doi:10.1093/stmcls/sxag023

Transplantation of human stem cell-derived cone photoreceptors partially restores vision in aged rd1 mice with advanced retinal degeneration.

Journal: Stem cells (Dayton, Ohio)

In common: mouse, cellular / molecular, 1 reference

[4] doi: [code]

Transcript architecture predetermines m6A remodeling and sensory neuron vulnerability in chemotherapy-induced peripheral neuropathy

Journal: bioRxiv : the preprint server for biology

In common: mouse, cellular / molecular, 1 reference

[5] doi:10.1126/sciadv.aeb7558

An engineered insulin analog with dual insulin and IGF-1 receptor agonism and distinct signaling.

Journal: Science advances

In common: mouse, cellular / molecular, 1 reference

[6] doi:10.21203/rs.3.rs-9474472/v1 [code]

Donor Microbiota Metabolic Capacity Determines Engraftment Dynamics and Modulates Gut–Brain Signaling in Recipient Mice

Journal: Research Square (preprint)

In common: mouse, cellular / molecular, 1 reference

[7] doi:10.1186/s40478-026-02388-7

Galectin-3 is elevated in Müller glia in human glaucomatous eyes and ocular hypertensive rat eyes and associated with phagocytosing states.

Journal: Acta neuropathologica communications

In common: cellular / molecular, 1 reference

[8] doi:10.1242/jcs.264529

Increased Glycine-N-methyltransferase expression disrupts light-dependent gene expression rhythms in the Drosophila eye.

Journal: Journal of cell science

In common: cellular / molecular, 1 reference

[9] doi:10.1038/s44319-026-00858-6

Ligand-independent EPHA2 signaling sustains neural progenitors via ECSIT and NAD<sup/>.

Journal: EMBO reports

In common: mouse, 1 reference

[10] doi:10.3390/metabo16080541

Spatial Metabolomics and Single-Cell Virtual Knockout Screening Reveal Solanesol Improves Parkinson's Disease-like Pathology Based on Lipid Inflammation Mechanism.

Journal: Metabolites

In common: cellular / molecular, 1 reference

Contribute

The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.

Request its removal

To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).

Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.

Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.

Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.