Evidence map›Paper›PMID 33680286›Full record

ArticleOxidative medicine and cellular longevity2021

General Control of Amino Acid Synthesis 5-Like 1-Mediated Acetylation of Manganese Superoxide Dismutase Regulates Oxidative Stress in Diabetic Kidney Disease.

Tingting Lv, Yao Lu, Yi Liu, Hong Feng, Chensheng Li, Wei Sheng, Zhengguo Cui, Suwei Zhu, Xia Gu, Zhe Yang and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2021. 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
6.9field-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

18 citing papers in PubMed, 55 citations in OpenAlex.

  1. Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026
    Review
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  16. GPER-dependent estrogen signaling increases cardiac GCN5L1 expression.American journal of physiology. Heart and circulatory physiology · 2022
    Article
  17. Sirtuin Family and Diabetic Kidney Disease.Frontiers in endocrinology · 2022
    Review
  18. Article
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

11 authors at 2 institutions in 2 countries.

Tingting LvSchool of Medicine, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.ORCID https://orcid.org/0000-0002-8976-3703
Yao LuSchool of Medicine, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Yi LiuDepartment of Pulmonary and Critical Care Medicine, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Hong FengCancer Centre, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Chensheng LiDepartment of Gastrointestinal Surgery, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Wei ShengCancer Centre, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Zhengguo CuiDepartment of Public Health, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Suwei ZhuSchool of Medicine, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Xia GuSchool of Medicine, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Zhe YangCancer Centre, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.ORCID https://orcid.org/0000-0003-4082-6088
Qiang WanDepartment of Endocrinology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.ORCID https://orcid.org/0000-0001-9173-2941
Shandong University · CNUniversity of Toyama · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic kidney disease (DKD) is the major cause of end-stage renal disease (ESRD). In the past few decades, there has been a large amount of evidence to highlight the pivotal role of oxidative stress in the development and progression of DKD. However, the detailed molecular mechanisms are not fully elucidated. A new sight has been established that the mitochondrial acetyltransferase GCN5L1 participates in cellular redox homeostasis maintenance in DKD. Firstly, we found that the expression of GCN5L1 is significantly elevated both in human and mouse kidney tissues with DKD and in hyperglycemic renal tubular epithelial cells (TECs), while deletion of GCN5L1 could effectively ameliorate oxidative stress-induced renal injury in DKD. Furthermore, deletion of GCN5L1 could reduce MnSOD acetylation on lysine 68 and activate its activity, thereby scavenging excessive ROS and relieving oxidative stress-induced renal inflammation and fibrosis. In general, GCN5L1-mediated acetylation of MnSOD exacerbated oxidative stress-induced renal injury, suggesting that GCN5L1 might be a potential intervention target in DKD.

Indexed as

Oxidative StressAcetylationAnimalsCell LineDiabetic NephropathiesDisease Models, AnimalDown-RegulationEpithelial CellsEpithelial-Mesenchymal TransitionGlucoseHumansInflammationKidney TubulesLysineMaleMiceBLOC1S1 protein, humanBLOC1S1 protein, mouseGlucoseLysineMitochondrial ProteinsNerve Tissue ProteinsReactive Oxygen SpeciesStreptozocinSuperoxide Dismutase

Identifiers

PMID33680286
PMCPMC7906818
OpenAlexW3132591762

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.