ArticleCurrent eye research2016
Mitochondrial Profile and Responses to TGF-β Ligands in Keratoconus.
Article in Current eye research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.
What it found
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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.
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Who cites it
16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.
- The candidate proteins associated with keratoconus: A meta-analysis and bioinformatic analysis.PloS one · 2024Pooled it
- Systematically Displaying the Pathogenesis of KeratoconusFrontiers in medicine · 2021Pooled it
- Integrated multi-omics analysis combined with clinical validation reveals that HLA-DRB5 and ODAPH are causal risk genes for keratoconus.Scientific reports · 2026Article
- Transforming growth factor-β3 attenuates septic cardiomyopathy by reversing cardiomyocyte metabolic reprogramming through Smad7 signaling.Molecular and cellular biochemistry · 2026Article
- The role of transforming growth factor beta-1 (TGF-β1) in the development of fibrosis in keratoconus.Irish journal of medical science · 2025Article
- Investigating prolactin-induced protein and its role in modulating the metabolic state of the keratoconus microenvironment.Experimental eye research · 2025Review
- Shared molecular profiles of post-laser vision correction ectasia and keratoconus with key differences inFrontiers in molecular biosciences · 2025Article
- Inherited mitochondrial dysfunction triggered by OPA1 mutation impacts the sensory innervation fibre identity, functionality and regenerative potential in the cornea.Scientific reports · 2024Article
- Identification of hub genes and molecular pathways in keratoconus by integrating bioinformatics and literature mining at the RNA level.International ophthalmology · 2024Article
- Lack of Elevated Expression of TGFβ3 Contributes to the Delay of Epithelial Wound Healing in Diabetic Corneas.Investigative ophthalmology & visual science · 2024Article
- Characteristics of Autophagy-Related Genes, Diagnostic Models, and Their Correlation with Immune Infiltration in Keratoconus.Journal of inflammation research · 2023Article
- Review
- Transcriptional profiling of corneal stromal cells derived from patients with keratoconus.Scientific reports · 2019Article
- Analysis of sphingolipids in human corneal fibroblasts from normal and keratoconus patients.Journal of lipid research · 2017Article
- Quercetin and the ocular surface: What we know and where we are going.Experimental biology and medicine (Maywood, N.J.) · 2017Review
- Differential Effects of Hormones on Cellular Metabolism in Keratoconus In Vitro.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
purposeKeratoconus (KC) is a complex corneal dystrophy with multifactorial etiology. Previous studies have shown evidence of mitochondrial abnormalities in KC; however, the exact cause of these abnormalities remains unknown. The aim of this study was to identify if transforming growth factor-β (TGF-β) isoforms play a role in the regulation of mitochondrial proteins in human KC cells (HKC). MATERIALS AND
methodsHuman corneal fibroblasts (HCF) and HKC were isolated and cultured for 4 weeks in three different conditions: (a) CONTROL: MEM + 10%FBS, (b) MEM + 10%FBS + TGF-β1 and (c) MEM + 10%FBS + TGF-β3. All samples were processed for mitochondrial damage analysis using real-time PCR.
resultsWe quantified and analyzed 84 mitochondrial and five housekeeping genes in HCFs and HKCs. Our data showed that when TGF-β1 and/or TGF-β3 were compared with control in HCFs, nine genes were significantly different; however, no genes were significantly regulated by the TGF-β isoforms in HKCs. Significant differences were also seen in seven genes when HFCs were compared with HKCs, in all three conditions.
conclusionsOverall, our data support the growing consensus that mitochondrial dysfunction is a key player in KC disease. These in vitro data show clear links between mitochondrial function and TGF-β isoforms, with TGF-β1 severely disrupting KC-mitochondrial function, while TGF-β3 maintained it, thus suggesting that TGF-β may play a role in KC-disease treatment.
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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.