Evidence map›Paper›PMID 35089329›Full record

ArticleInvestigative ophthalmology & visual science2022

MiR-223-3p Regulates Autophagy and Inflammation by Targeting ATG16L1 in Fusarium solani-Induced Keratitis.

Hanfeng Tang, Yi Lin, Liwei Huang, Jianzhang Hu

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.3field-weighted citation impact, top 5% of its field
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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. [Tongdu Zhiyu Acupuncture Improves Post-Stroke Depression by Upregulating miR-223-3p and Inhibiting NLRP3 Inflammasome: A Clinical Study].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026
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  14. Tear Film MicroRNAs as Potential Biomarkers: A Review.International journal of molecular sciences · 2023
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  16. Autophagy in the normal and diseased cornea.Experimental eye research · 2022
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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

4 authors at 2 institutions in 1 country.

Hanfeng TangDepartment of Ophthalmology, Fujian Medical University Union Hospital, Fu Zhou, China.
Yi LinDepartment of Ophthalmology, Fujian Medical University Union Hospital, Fu Zhou, China.
Liwei HuangDepartment of Ophthalmology, Fujian Medical University Union Hospital, Fu Zhou, China.
Jianzhang HuDepartment of Ophthalmology, Fujian Medical University Union Hospital, Fu Zhou, China.
Fujian Medical University · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Increasing evidence suggested that microRNAs (miRs) are implicated in the regulation of the inflammatory response and autophagy in multiple diseases. The present study aimed to explore the effect of miR-223-3p on inflammation and autophagy in fungal keratitis (FK). Methods: An FK mouse model was established, and primary corneal stromal cells were isolated by inoculation with Fusarium solani. The expression of miR-223-3p was determined by quantitative RT-PCR. Subsequently, the target gene of miR-223-3p was identified by a dual-luciferase reporter assay. The levels of miR-223-3p were altered by transfecting miR agomir/antagomir to evaluate its effects. Slit-lamp biomicroscopy and hematoxylin and eosin staining were employed to detect corneal damage. The levels of autophagy were assessed by immunofluorescence, Western blotting, mRFP-GFP-LC3 fluorescence microscopy, and electron microscopy. In addition, inflammation was demonstrated by determining the proinflammatory mediators IL-1β and TNF-ɑ. Results: Our data suggested that miR-223-3p was increased and that autophagic flux was impaired in mouse FK. Then, we confirmed that autophagy-related gene 16L1 (ATG16L1) was a potential target of miR-223-3p and that this miR negatively regulated the expression of ATG16L1. The inhibition of miR-223-3p attenuated inflammation in FK, reduced P62 expression, and increased the ratio of LC3-II/LC3-I, whereas the overexpression of miR-223-3p displayed the opposite results. Conclusions: Taken together, miR-223-3p might regulate autophagy via targeting ATG16L1 in experimental F. solani keratitis and is associated with the inflammatory response. MiR-223-3p might be a potential therapeutic target for FK.

Indexed as

Gene Expression RegulationAnimalsAutophagyCells, CulturedDisease Models, AnimalEye Infections, FungalFusariumKeratitisMiceMice, Inbred BALB CMicroRNAsRNAMicroRNAsMIRN223 microRNA, mouseRNA

Identifiers

PMID35089329
PMCPMC8802027
OpenAlexW4210345141

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.