ReviewCells2021
Mitochondrial Dysfunction and Mitophagy in Fuchs Endothelial Corneal Dystrophy.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Transcriptomic meta-analysis reveals ERRα-mediated oxidative phosphorylation is downregulated in Fuchs' endothelial corneal dystrophy.PloS one · 2023Pooled it
- Mitochondrial Control of Myelination, Bioenergetics, Oxidative Stress, and the Pathogenesis of Optic Neuropathies.International journal of molecular sciences · 2026Review
- Crosstalk between endoplasmic reticulum stress and mitochondrial homeostasis: A new perspective on ophthalmic disease treatment.Journal of cell communication and signaling · 2026Review
- Metabolic and redox adaptations of the corneal endothelium: From metabolic plasticity to therapeutic opportunities.Redox biology · 2026Review
- Cross-Cohort Evidence of Editome Dysregulation and Cell Growth-Related IGFBP7 Recoding Driven by ADARB1 in Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2026Article
- Enhanced mitochondria-associated membrane formation in Fuchs endothelial corneal dystrophy: a novel link between endoplasmic reticulum stress and mitochondrial dysfunction.Japanese journal of ophthalmology · 2026Article
- TAZ (bioRxiv : the preprint server for biology · 2026Article
- Taurochenodeoxycholic Acid Activates Calcium Signaling to Protect Against Fuchs' Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2026Article
- A Murine Model of HSV-1-Induced Corneal Endotheliitis: Primary Infection, Latency, and Recurrence.Investigative ophthalmology & visual science · 2026Article
- Early Transcriptomic and Pathologic Changes of Col8a2 Mutant Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2026Article
- Autophagy in ocular diseases: from mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- Transcriptome analyses of human corneal endothelial cell lines derived from patients with Fuchs endothelial corneal dystrophy.Scientific reports · 2025Article
- Bioinformatic Analysis of the Value of Mitophagy and Immune Responses in Corneal Endothelial Dysfunction.Current issues in molecular biology · 2025Article
- The PERK-p38 MAPK Axis Drives Endoplasmic Reticulum Stress-Induced Apoptosis in Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2025Article
- Generation of a Mouse Model of Fuchs Endothelial Corneal Dystrophy by Knock-in of CTG Trinucleotide Repeat Expansion in the TCF4 Gene.Investigative ophthalmology & visual science · 2025Article
- Associations between measures of oestrogen exposure and severity of Fuchs endothelial corneal dystrophy.BMJ open ophthalmology · 2025Article
- A feasibility of computational drug screening for Fuchs endothelial corneal dystrophy.Scientific reports · 2025Article
- Article
- Iron-Sulfur Clusters and Iron Responsive Element Binding Proteins Mediate Iron Accumulation in Corneal Endothelial Cells in Fuchs Dystrophy.Investigative ophthalmology & visual science · 2025Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Fuchs endothelial corneal dystrophy (FECD) is a genetically complex, heterogenous, age-related degenerative disease of corneal endothelial cells (CEnCs), occurring in the fifth decade of life with a higher incidence in females. It is characterized by extracellular matrix (ECM) protein deposition called corneal guttae, causing light glare and visual complaints in patients. Corneal transplantation is the only treatment option for FECD patients, which imposes a substantial socioeconomic burden. In FECD, CEnCs exhibit stress-induced senescence, oxidative stress, DNA damage, heightened reactive oxygen species (ROS) production, mitochondrial damage, and dysfunction as well as sustained endoplasmic reticulum (ER) stress. Among all of these, mitochondrial dysfunction involving altered mitochondrial bioenergetics and dynamics plays a critical role in FECD pathogenesis. Extreme stress initiates mitochondrial damage, leading to activation of autophagy, which involves clearance of damaged mitochondria called auto(mito)phagy. In this review, we discuss the role of mitochondrial dysfunction and mitophagy in FECD. This will provide insights into a novel mechanism of mitophagy in post-mitotic ocular cell loss and help us explore the potential treatment options for FECD.
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What OpenQuestion holds
Registered trials
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.