Evidence map›Paper›PMID 36427396›Full record

ArticleRedox biology2022

FBXW7 alleviates hyperglycemia-induced endothelial oxidative stress injury via ROS and PARP inhibition.

Shenping Li, Junjie Deng, Dandan Sun, Shimei Chen, Xieyi Yao, Ning Wang, Jian Zhang, Qing Gu, Shuchang Zhang, Jing Wang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

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  13. PARP inhibition preserves cone photoreceptors in rd2 retina.Acta neuropathologica communications · 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

15 authors at 2 institutions in 1 country.

Shenping LiDepartment of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China; Department of Ophthalmology, Shanghai General Hospital, Shanghai, 200080, China.
Junjie DengDepartment of Ophthalmology, Shanghai General Hospital, Shanghai, 200080, China.
Dandan SunDepartment of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China; Department of Ophthalmology, Shanghai General Hospital, Shanghai, 200080, China.
Shimei ChenDepartment of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China; Department of Ophthalmology, Shanghai General Hospital, Shanghai, 200080, China.
Xieyi YaoDepartment of Ophthalmology, Shanghai General Hospital, Shanghai, 200080, China.
Ning WangDepartment of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China; National Clinical Research Center for Eye Diseases, Shanghai, 200080, China; Department of Ophthalmology, Shanghai General Hospital, Shanghai, 200080, China.
Jian ZhangDepartment of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China; National Clinical Research Center for Eye Diseases, Shanghai, 200080, China; Department of Ophthalmology, Shanghai General Hospital, Shanghai, 200080, China.
Qing GuDepartment of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China; National Clinical Research Center for Eye Diseases, Shanghai, 200080, China; Shanghai Key Laboratory of Ocular Fundus Diseases, Shanghai, 200080, China.
Shuchang ZhangDepartment of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China; Department of Ophthalmology, Shanghai General Hospital, Shanghai, 200080, China.
Jing WangDepartment of Ophthalmology, Shanghai General Hospital, Shanghai, 200080, China.
Shaopin ZhuDepartment of Ophthalmology, Shanghai General Hospital, Shanghai, 200080, China.
Hong ZhuDepartment of Ophthalmology, Shanghai General Hospital, Shanghai, 200080, China; Shanghai Engineering Center for Visual Science and Photomedicine, Shanghai, 200080, China.
Huiming LiDepartment of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
Xun XuDepartment of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China; National Clinical Research Center for Eye Diseases, Shanghai, 200080, China; Department of Ophthalmology, Shanghai General Hospital, Shanghai, 200080, China; Shanghai Key Laboratory of Ocular Fundus Diseases, Shanghai, 200080, China; Shanghai Engineering Center for Visual Science and Photomedicine, Shanghai, 200080, China. Electronic address: drxuxun@sjtu.edu.cn.
Fang WeiDepartment of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China; National Clinical Research Center for Eye Diseases, Shanghai, 200080, China; Department of Ophthalmology, Shanghai General Hospital, Shanghai, 200080, China; Shanghai Key Laboratory of Ocular Fundus Diseases, Shanghai, 200080, China; Shanghai Engineering Center for Visual Science and Photomedicine, Shanghai, 200080, China. Electronic address: weifang73@hotmail.com.
Shanghai First People's Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic retinopathy (DR) and other diabetic vascular complications are the leading cause of death and disability in patients with suboptimum glycemic control. In the pathogenesis of diabetic vascular diseases, hyperglycemia-induced oxidative stress, DNA damage, and poly-ADP-ribose-polymerase (PARP) hyperactivation play important roles in endothelial cell impairment. Adipose differentiation-related protein FBXW7 was reported to regulate PGC-1α stability and mitochondrial homeostasis. Here, we investigated the role and mechanism of FBXW7 in repairing endothelial oxidative stress injuries under hyperglycemic conditions. FBXW7 promoted the hampered activity of homologous recombination and non-homologues end joining pathway for repairing DNA double-strand breaks damage, an initiating factor for PARP hyperactivation and diabetic vascular complications. The abundant mobilization of DNA damage repair mediated by FBXW7 suppressed PARP activation, leading to downregulation of PARP expression and activity in both human endothelial cells and diabetic rat retinas. This provided a new method for PARP inhibition, superior to PARP inhibitors for treating diabetic vascular complication. Furthermore, FBXW7 rescued downregulated NAD+ levels and ameliorated mitochondrial dysfunction, thereby reducing superoxide production under hyperglycemic conditions. These effects reversed oxidative injury and vascular leakage in diabetic rat retina, providing a potential future treatment strategy.

Indexed as

Diabetic AngiopathiesHyperglycemiaAnimalsEndothelial CellsF-Box-WD Repeat-Containing Protein 7HumansOxidative StressPoly(ADP-ribose) Polymerase InhibitorsRatsReactive Oxygen SpeciesF-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanFbxw7 protein, ratPoly(ADP-ribose) Polymerase InhibitorsReactive Oxygen SpeciesDiabetic retinopathyDNA damageEndothelial cellMitochondriaOxidative stress

Identifiers

PMID36427396
PMCPMC9692029
OpenAlexW4309336551

What OpenQuestion holds

Textmetadata
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.