Evidence map›Paper›PMID 33714955›Full record

ArticleAging2021

Activation of ATF4 triggers trabecular meshwork cell dysfunction and apoptosis in POAG.

Ying Ying, Ran Xue, Yangfan Yang, Sarah X Zhang, Hui Xiao, Huazhang Zhu, Jingming Li, Guo Chen, Yiming Ye, Minbin Yu and 2 more

Open access · greenAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 45 citations in OpenAlex.

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  10. Protein misfolding and mitochondrial dysfunction in glaucoma.Frontiers in cell and developmental biology · 2025
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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

12 authors at 4 institutions in 2 countries.

Ying YingDepartment of Physiology, Shenzhen University Health Science Center, Shenzhen University, Shenzhen, Guangdong, China.
Ran XueState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, Guangdong, China.
Yangfan YangState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, Guangdong, China.
Sarah X ZhangDepartment of Ophthalmology and Ross Eye Institute, University at Buffalo, State University of New York, Buffalo, NY 14209, USA.
Hui XiaoState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, Guangdong, China.
Huazhang ZhuDepartment of Physiology, Shenzhen University Health Science Center, Shenzhen University, Shenzhen, Guangdong, China.
Jingming LiDepartment of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University College of Medicine, Xi an, Shanxi, China.
Guo ChenState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, Guangdong, China.
Yiming YeState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, Guangdong, China.
Minbin YuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, Guangdong, China.
Xing LiuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, Guangdong, China.
Yimin ZhongState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, Guangdong, China.
Sun Yat-sen University · CNShenzhen University Health Science Center · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CNUniversity at Buffalo, State University of New York · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary open angle glaucoma (POAG) is the leading cause of irreversible blindness. Dysfunction of the trabecular meshwork (TM), resulting in decreased outflow of aqueous humor and increased intraocular pressure (IOP), plays an important role in the pathogenesis of POAG. However, the underlying mechanisms still remain unclear. In this study, we demonstrated that the eIF2-α/ATF4/CHOP branch of unfolded protein response (UPR) was activated in human trabecular meshwork cells (HTMCs) upon tert-butyl hydroperoxide (TBHP) exposure. Inhibition of ATF4 ameliorated TBHP-induced apoptosis and inflammatory cytokine production, while ectopic expression of ATF4 increased the expression of endothelial leukocyte adhesion molecule (ELAM)-1 and IL-8 in HTMCs. Furthermore, we found that ATF4 inhibition reduced tunicamycin-induced caspase-3 activation, ROS production, ELAM-1 expression, and HTMCs phagocytosis impairment. By an

Indexed as

Activating Transcription Factor 4AnimalsApoptosisEndoplasmic Reticulum StressGlaucoma, Open-AngleHumansMiceMice, Inbred C57BLOxidative StressTrabecular MeshworkActivating Transcription Factor 4activating transcription factor 4endoplasmic reticulum stressoxidative stressprimary open angle glaucomatrabecular meshwork

Identifiers

PMID33714955
PMCPMC8034903
OpenAlexW3133526397

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.