Evidence map›Paper›PMID 35775122›Full record

ArticleJournal of cellular and molecular medicine2022

Lysine-specific demethylase 1 aggravated oxidative stress and ferroptosis induced by renal ischemia and reperfusion injury through activation of TLR4/NOX4 pathway in mice.

Ruikang Feng, Yufeng Xiong, Yourong Lei, Qin Huang, Hao Liu, Xiaojie Zhao, Zhiyuan Chen, Hui Chen, Xiuheng Liu, Lei Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
4.1field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.

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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

11 authors at 1 institution in 1 country.

Ruikang FengDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Yufeng XiongDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.ORCID 0000-0001-9810-1691
Yourong LeiDepartment of infection prevention and control, Renmin Hospital of Wuhan University, Wuhan, China.
Qin HuangDepartment of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, China.
Hao LiuDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Xiaojie ZhaoDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Zhiyuan ChenDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Hui ChenDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Xiuheng LiuDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.ORCID 0000-0003-3882-2715
Lei WangDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Xiaodong WengDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Wuhan University · CN

Funding

National Natural Science Foundation of China 82000639
6 · The paper itself

Abstract

Acute kidney injury (AKI) is mainly caused by renal ischaemia reperfusion injury (IRI). Lots of evidence suggests that ferroptosis and oxidative stress play the vital role in renal IRI. However, the specific mechanism of renal IRI has not been fully elucidated. lysine-specific demethylase 1 (LSD1) has been shown to regulate the pathogenesis of kidney disease. In this study, we firstly found that LSD1 was positively related to renal IRI. TCP, a classical LSD1 inhibitor, could alleviate tissue damage induced by renal IRI. Inhibition of LSD1 with either TCP or LSD1 knockdown could alleviate ferroptosis and oxidative stress caused by IRI both in vivo and in vitro. Furthermore, the results showed that suppression of LSD1 decreased the expression of TLR4/NOX4 pathway in HK-2 cells subjected to H/R. With the si-RNA against TLR4 or NOX4, it showed that the silence of TLR4/NOX4 reduced oxidative stress and ferroptosis in vitro. Moreover, to demonstrate the crucial role of TLR4/NOX4, TLR4 reduction, mediated by inhibition of LSD1, was compensated through delivering the adenovirus carrying TLR4 in vitro. The results showed that the compensation of TLR4 blunted the alleviation of oxidative stress and ferroptosis, induced by LSD1 inhibition. Further study showed that LSD1 activates TLR4/NOX4 pathway by reducing the enrichment of H3K9me2 in the TLR4 promoter region. In conclusion, our results demonstrated that LSD1 inhibition blocked ferroptosis and oxidative stress caused by renal IRI through the TLR4/NOX4 pathway, indicating that LSD1 could be a potential therapeutic target for renal IRI.

Indexed as

Acute Kidney InjuryFerroptosisReperfusion InjuryAnimalsHistone DemethylasesIschemiaKidneyLysineMiceNADPH Oxidase 4Oxidative StressSignal TransductionToll-Like Receptor 4Histone DemethylasesKDM1a protein, mouseLysineNADPH Oxidase 4Nox4 protein, mouseTlr4 protein, mouseToll-Like Receptor 4ferroptosisischaemia and reperfusion injuryLSD1oxidative stress

Identifiers

PMID35775122
PMCPMC9344828
OpenAlexW4283742404

What Socratic 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 Socratic graph.