Evidence map›Paper›PMID 33722625›Full record

ArticleFree radical biology & medicine2021

Aging lens epithelium is susceptible to ferroptosis.

Zongbo Wei, Caili Hao, Jingru Huangfu, Ramkumar Srinivasagan, Xiang Zhang, Xingjun Fan

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

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  7. TRIM69 alleviates ultraviolet B irradiation-induced ferroptosis by regulating p53 in human lens epithelial cells.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026
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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

6 authors at 3 institutions in 2 countries.

Zongbo WeiDepartment of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University, Augusta, Georgia.
Caili HaoDepartment of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University, Augusta, Georgia.
Jingru HuangfuDepartment of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University, Augusta, Georgia; Department of Ophthalmology, Chongqing Medical University, Chongqing, China.
Ramkumar SrinivasaganDepartment of Pharmacology, Case Western Reserve University, Cleveland, OH, United States.
Xiang ZhangGenomics, Epigenomics and Sequencing Core, Department of Environmental and Public Health Sciences, University of Cincinnati, Cincinnati, OH, United States.
Xingjun FanDepartment of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University, Augusta, Georgia. Electronic address: xfan@augusta.edu.
Augusta University · USCase Western Reserve University · USUniversity of Cincinnati · US

Funding

Module 3: Gene Expression/ProteomicsP30EY031631 · NEI · AUGUSTA UNIVERSITY · PI Xingjun Fan · 2020 to 2026
$3.6M
Mechanisms and consequences of impaired glutathione homeostasis in the aging Lens.R01EY028158 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI Xingjun Fan · 2018 to 2026
$3.1M
NEI NIH HHS P30 EY031631NEI NIH HHS R01 EY028158
6 · The paper itself

Abstract

Age-related cataracts (ARC) are the primary cause of blindness worldwide, and oxidative stress is considered the central pathogenesis of age-related cataractogenesis. Interestingly, ample evidence suggests that there is no remarkable apoptosis present in aged and cataractous human lenses despite the profound disruption of redox homeostasis, raising an essential question regarding the existence of other cell death mechanisms. Here we sought to explore the lens epithelial cell's (LEC) susceptibility to ferroptosis after documentation has concluded that aged and cataractous human lenses manifest with increased reactive oxygen species (ROS) formation, elevated lipid peroxidation, and accumulative intracellular redox-active iron, constituting the three hallmarks of ferroptosis during aging and cataractogenesis. Here we show that very low concentrations of system X

Indexed as

FerroptosisAgingAnimalsEpitheliumLipid PeroxidationMicePhospholipid Hydroperoxide Glutathione PeroxidasePhospholipid Hydroperoxide Glutathione PeroxidaseAge-related cataractAgingCataractogenesisFerroptosisGlutathione homeostasisIron homeostasisLipid peroxidationReactive oxygen species (ROS)

Identifiers

PMID33722625
PMCPMC8096685
OpenAlexW3137053813

What OpenQuestion holds

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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.