Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Antioxidant MitoQ increases viability of human corneal endothelial cells with congenital hereditary endothelial dystrophy-associated SLC4A11 mutations.

Ophthalmic genetics - 1 Apr 2025

Peshkar-Kulkarni Saloni, Chung Doug D, Aldave Anthony J

Abstract excerpt

PURPOSE: To assess the impact of MitoQ, a mitochondria-targeted antioxidant, on viability of human corneal endothelial cell (hCEnC) lines expressing SLC4A11 mutations associated with congenital hereditary endothelial dystrophy (CHED) and Fuchs endothelial corneal dystrophy type 4 (FECD4). METHODS: SLC4A11 wildtype (SLC4A11WT) and mutant (SLC4A11MU) hCEnC lines were created to express either SLC4A11 variant 2 (V2)...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Anion Transport Proteins
Share to Antioxidants

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Antiporters

Share to Corneal Dystrophies, Hereditary

Share to Endothelium, Corneal

Share to Fuchs' Endothelial Dystrophy

Share to Organophosphorus Compounds

Share to Ubiquinone

Source

Open in PubMed Open full text

Identifiers

PMID: 39834031
DOI: 10.1080/13816810.2025.2450455
PMCID: PMC12003074

Genes

SLC4A11

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Antioxidant MitoQ increases viability of human corneal endothelial cells with congenital hereditary endothelial dystrophy-associated SLC4A11 mutations.PMID 39834031Read ↗

SLC4A11 depletion impairs NRF2 mediated antioxidant signaling and increases reactive oxygen species in human corneal endothelial cells during oxidative stressSemantic proximity Read ↗

Restoration of Mitochondrial Integrity, Telomere Length, and Sensitivity to Oxidation by In Vitro Culture of Fuchs' Endothelial Corneal Dystrophy CellsSemantic proximity Read ↗

Investigation of the functional impact of CHED- and FECD4-associated SLC4A11 mutations in human corneal endothelial cells.Semantic proximity Read ↗

Rescuing cellular function in Fuchs endothelial corneal dystrophy by healthy exogenous mitochondrial internalizationSemantic proximity Read ↗

Energy Shortage in Human and Mouse Models of SLC4A11-Associated Corneal Endothelial Dystrophies.Semantic proximity Read ↗

Energy Shortage in Human and Mouse Models of <i>SLC4A11</i> -Associated Corneal Endothelial DystrophiesSemantic proximity Read ↗

<i>TCF4</i> trinucleotide repeat expansions and UV irradiation increase susceptibility to ferroptosis in Fuchs endothelial corneal dystrophySemantic proximity Read ↗

TCF4 trinucleotide repeat expansions and UV irradiation increase susceptibility to ferroptosis in Fuchs endothelial corneal dystrophySemantic proximity Read ↗

Human SLC4A11-C functions as a DIDS-stimulatable H⁺(OH⁻) permeation pathway: partial correction of R109H mutant transport.Semantic proximity Read ↗

Corneal dystrophy-causing SLC4A11 mutants: suitability for folding-correction therapy.Semantic proximity Read ↗

p53-Regulated Increase in Oxidative-Stress–Induced Apoptosis in Fuchs Endothelial Corneal Dystrophy: A Native Tissue ModelSemantic proximity Read ↗

Selective effects of estradiol on human corneal endothelial cellsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.