ArticleMolecular biology reports2024
Mir-204-5p alleviates mitochondrial dysfunction by targeting IGFBP5 in diabetic cataract.
Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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Who cites it
3 citing papers in PubMed.
- METTL14 Ameliorates Mitochondrial Dysfunction and Autophagy in Lens Epithelial Cells of Diabetic Cataracts via m6A Modification of RPL3.The Kaohsiung journal of medical sciences · 2026Article
- Endothelial progenitor cell derived extracellular vesicles promotes wound healing in diabetic mice via activating mobilization and neovascularization.Cell biology and toxicology · 2026Article
- The IL-36γ/PEDF/PPARγ signalling pathway plays an anti-inflammatory role in Candida albicans keratitis.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundCataract contributes to visual impairment worldwide, and diabetes mellitus accelerates the formation and progression of cataract. Here we found that the expression level of miR-204-5p was diminished in the lens epithelium with anterior lens capsule of cataract patients compared to normal donors, and decreased more obviously in those of diabetic cataract (DC) patients. However, the contribution and mechanism of miR-204-5p during DC development remain elusive. METHODS AND
resultThe mitochondrial membrane potential (MMP) was reduced in the lens epithelium with anterior lens capsule of DC patients and the H2O2-induced human lens epithelial cell (HLEC) cataract model, suggesting impaired mitochondrial functional capacity. Consistently, miR-204-5p knockdown by the specific inhibitor also attenuated the MMP in HLECs. Using bioinformatics and a luciferase assay, further by immunofluorescence staining and Western blot, we identified IGFBP5, an insulin-like growth factor binding protein, as a direct target of miR-204-5p in HLECs. IGFBP5 expression was upregulated in the lens epithelium with anterior lens capsule of DC patients and in the HLEC cataract model, and IGFBP5 knockdown could reverse the mitochondrial dysfunction in the HLEC cataract model.
conclusionsOur results demonstrate that miR-204-5p maintains mitochondrial functional integrity through repressing IGFBP5, and reveal IGFBP5 may be a new therapeutic target and prognostic factor for DC.
Indexed as
Identifiers
38874707What Socratic 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 Socratic graph.