ArticleMolecular medicine reports2018
miR-24-p53 pathway evoked by oxidative stress promotes lens epithelial cell apoptosis in age-related cataracts.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- A comprehensive investigation of identifying miRNA biomarkers and their potential role in age-related cataract by meta-analysis and bioinformatics analysis.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2025Pooled it
- A three-pronged strategy with minimalist nattokinase nanocomposite eye drops breaks the vicious cycle in ultraviolet-B-induced cataract.Journal of nanobiotechnology · 2026Article
- A Pilot Investigation of Circulating miRNA Expression in Individuals Exposed to Aluminum and Welding Fumes.Current issues in molecular biology · 2025Article
- MicroRNAs as Regulators of Radiation-Induced Oxidative Stress.Current issues in molecular biology · 2024Review
- Platelet microparticles influence gene expression and modulate biological activities of chronic myeloid leukemia cells (K562).Molecular biology reports · 2024Article
- A bibliometric and visualized analysis of the pathogenesis of cataracts from 1999 to 2023.Heliyon · 2024Article
- Alternate Causes for Pathogenesis of Exfoliation Glaucoma, a Multifactorial Elastotic Disorder: A Literature Review.Current issues in molecular biology · 2022Review
- Versatile role of miR-24/24-1*/24-2* expression in cancer and other human diseases.American journal of translational research · 2022Review
- Article
- miR-24 and its target gene Prdx6 regulate viability and senescence of myogenic progenitors during aging.Aging cell · 2021Article
- Micro RNAs in Regulation of Cellular Redox Homeostasis.International journal of molecular sciences · 2021Review
- The Potential Role of Zinc Oxide Nanoparticles in MicroRNAs Dysregulation in STZ-Induced Type 2 Diabetes in Rats.Biological trace element research · 2020Article
- Long non-coding RNA ANRIL alleviates HAging · 2020Article
- Expression of miR-34a in cataract rats and its related mechanism.Experimental and therapeutic medicine · 2020Article
- 5-Azacytydine and resveratrol reverse senescence and ageing of adipose stem cells via modulation of mitochondrial dynamics and autophagy.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA-24 (miR-24) serves an important role in cell proliferation, migration and inflammation in various types of disease. In the present study, the biological function and molecular mechanism of miR‑24 was investigated in association with the progression of age‑associated cataracts. To the best of our knowledge the present study is the first to report that the expression of miR‑24 was significantly increased in human anterior lens capsules affected by age‑associated cataracts as well as lens epithelial cells (LECs) exposed to oxidative stress. Overexpression of miR‑24 induced p53 expression and p53 was verified as a direct target of miR‑24. Overexpression of miR‑24 enhanced LEC death by directly targeting p53. The present study revealed that oxidative stress induced the upregulation of miR‑24 and enhanced LEC death by directly targeting p53. These results suggest that the miR‑24‑p53 signaling pathway is involved in a novel mechanism of age‑associated cataractogenesis and miR‑24 may be a useful therapeutic target for age-associated cataracts.
Indexed as
Identifiers
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.