Evidence map›Paper›PMID 38721513›Full record

ArticleInternational journal of ophthalmology2024

Overexpression of TRPV1 activates autophagy in human lens epithelial cells under hyperosmotic stress through Ca

Liu-Hui Huang, Jiao Lyu, Sheng Chen, Ting-Yi Liang, Yu-Qing Rao, Ping Fei, Jing Li, Hai-Ying Jin, Pei-Quan Zhao

Abstract read
In one paragraph

Article in International journal of ophthalmology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–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

4 citing papers in PubMed.

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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

9 authors.

Liu-Hui HuangDepartment of Ophthalmology, Shanghai Xinhua Hospital Affiliated with Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.
Jiao LyuDepartment of Ophthalmology, Shanghai Xinhua Hospital Affiliated with Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.
Sheng ChenShenzhen Eye Hospital, Shenzhen Key Laboratory of Ophthalmology, Affiliated Shenzhen Eye Hospital of Jinan University, Shenzhen 518040, Guangdong Province, China.
Ting-Yi LiangDepartment of Ophthalmology, Shanghai Xinhua Hospital Affiliated with Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.
Yu-Qing RaoDepartment of Ophthalmology, Shanghai Xinhua Hospital Affiliated with Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.
Ping FeiDepartment of Ophthalmology, Shanghai Xinhua Hospital Affiliated with Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.
Jing LiDepartment of Ophthalmology, Shanghai Xinhua Hospital Affiliated with Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.
Hai-Ying JinDepartment of Ophthalmology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Pei-Quan ZhaoDepartment of Ophthalmology, Shanghai Xinhua Hospital Affiliated with Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo explore whether autophagy functions as a cellular adaptation mechanism in lens epithelial cells (LECs) under hyperosmotic stress.

methodsLECs were treated with hyperosmotic stress at the concentration of 270, 300, 400, 500, or 600 mOsm for 6, 12, 18, 24h

resultsThe hyperosmotic stress activated autophagy in a pressure- and time-dependent manner in LECs. Beclin 1 protein expression and conversion of LC3B II to LC3B I increased, whereas sequestosome-1 (SQSTM1) protein expression decreased. Transient Ca

conclusionA combination of hyperosmotic stress and autophagy inhibition may be a promising approach to decrease the number of LECs in the capsular bag and pave the way for improving prevention of posterior capsular opacification and capsular fibrosis.

Indexed as

apoptosisautophagycataracthyperosmotic stresslens epithelial cellposterior capsular opacificationtransient receptor potential vanilloid 1

Identifiers

PMID38721513
PMCPMC11074167

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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.