Evidence map›Paper›PMID 29299142›Full record

ArticleOncotarget2017

MicroRNA-34a promotes mitochondrial dysfunction-induced apoptosis in human lens epithelial cells by targeting Notch2.

Fan Fan, Jianhui Zhuang, Peng Zhou, Xin Liu, Yi Luo

Abstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. 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 · 2025
    Pooled it
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  7. Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
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  18. The Role of MicroRNAs in Mitochondria-Mediated Eye Diseases.Frontiers in cell and developmental biology · 2021
    Review
  19. Article
  20. Expression of miR-34a in cataract rats and its related mechanism.Experimental and therapeutic medicine · 2020
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Fan FanDepartment of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, China.
Jianhui ZhuangDepartment of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Peng ZhouParkway Health Hongqiao Medical Center, Shanghai, China.
Xin LiuDepartment of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, China.
Yi LuoDepartment of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeHuman lens epithelial cell (HLEC) apoptosis is a common pathogenic mechanism in age-related cataracts (ARC). While the function of microRNAs (miRNAs) in the eye is beginning to be explored using miRNA expression array, the role of miR-34a in regulating HLEC apoptosis remains unknown and requires further investigation.

methodsQuantitative reverse-transcript polymerase chain reaction (RT-PCR) was used to determine the expression level of miR-34a in cataractous and control samples. MiR-34a mimics and small interfering RNAs were transfected into SRA01/04. Cell apoptosis and oxidative stress were assessed by flow cytometry. The Dual-Luciferase Reporter Assay System was used to confirm whether miR-34a bound to the 3'-UTR of the target gene and blocked its activity. The potential roles of the identified target genes in apoptosis and mitochondria dysfunction were also evaluated.

resultsThe expression of miR-34a increased in lens epithelial samples of ARC compared with the transparent group (cataract 2.41±0.81 vs. control 1.20±0.44, P=0.005). In cultured SRA01/04, miR-34a increased reactive oxygen species production and induced apoptosis (early apoptosis: 45.55%±5.96% vs. 15.85%±4.93%, P<0.01; late apoptosis: 6.10%±2.67% vs. 0.95%±0.42%, P<0.01). Overexpression of miR-34a promoted mitochondria-mediated apoptosis through activation of caspase-9, disruption of the mitochondrial membrane potential, blocking of mitochondrial energy metabolism and enhancement of cytochrome C release. Furthermore, Notch1 and Notch2 were confirmed as putative targets of miR-34a, but only Notch2 was verified as the effector that triggered mitochondria-mediated apoptosis.

conclusionMicroRNA-34a is increased in the cataractous lens and triggers mitochondria-mediated apoptosis and oxidative stress by suppressing Notch2.

Indexed as

age-related cataractapoptosisHLECsmiR-34aNotch

Identifiers

PMID29299142
PMCPMC5746377

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Registered trials

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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.