Evidence map›Paper›PMID 29909462›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2018

Inhibition of semaphorin-3a suppresses lipopolysaccharide-induced acute kidney injury.

Xiaofang Tian, Hua Gan, Yizhou Zeng, Hongfei Zhao, Rong Tang, Yunfeng Xia

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2018. 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
1.4field-weighted citation impact, top 21% 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, 29 citations in OpenAlex.

  1. Article
  2. Article
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  4. Role of Semaphorin 3A in Kidney Development and Diseases.Diagnostics (Basel, Switzerland) · 2023
    Review
  5. Article
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  15. Review
  16. Review
  17. Semaphorin3A-Inhibitor Ameliorates Doxorubicin-Induced Podocyte Injury.International journal of molecular sciences · 2020
    Article
  18. Review
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 2 institutions in 1 country.

Xiaofang TianDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China.
Hua GanDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China.
Yizhou ZengDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China.
Hongfei ZhaoDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China.
Rong TangDepartment of Cardiology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China.
Yunfeng XiaDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China. xyf0920@126.com.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CN

Funding

Medical Research and Developmental Fund of the First Affiliated Hospital of Chongqing Medical University No. PYJJ2017-02Wu Jieping Medical Foundation No. 320.6750.16196
6 · The paper itself

Abstract

Semaphorin-3a (Sema3A), a soluble axon guidance cue, appears to play an important role in the development of acute kidney injury (AKI) and has been regarded as an early diagnostic marker to evaluate the progression of AKI. However, the role of Sema3A in sepsis-associated AKI remains unknown. In this study, lipopolysaccharide (LPS) was used to simulate sepsis-associated AKI and the role of Sema3A in LPS-induced AKI was investigated in vivo and in vitro. In our in vivo study, Sema3A was found in tubular epithelial cells (TECs), which presented a higher level after LPS treatment. Meanwhile, the results of our in vitro experiment showed that Sema3A was also elevated in NRK-52E cells treated by LPS. Notably, inhibition of Sema3A by (-)-epigallocatechin-3-gallate (EGCG) could significantly reduce kidney inflammation and apoptosis in mice. Likewise, EGCG intervention also ameliorated the inflammation and apoptosis of cells in vitro. Furthermore, our research also found that the Rac1/NF-κB p65 and JNK pathways were possibly involved in the Sema3A-mediated inflammation and apoptosis of TECs, respectively. Our findings suggest that Sema3A play a pathogenic role by promoting inflammation and apoptosis of TECs in LPS-induced AKI. It might serve as a useful treatment target in ameliorating sepsis-associated AKI. KEY MESSAGES: Sema3A is upregulated in LPS-induced AKI. Inhibition of Sema3A attenuates inflammation and apoptosis of TECs in LPS-induced AKI. Sema3A enhances the LPS-induced inflammation of TECs through the Rac1/NF-κB p65 pathway. Sema3A exacerbates the LPS-induced apoptosis of TECs through the JNK pathway.

Indexed as

Acute Kidney InjuryAnimalsApoptosisBiopsyCell LineCytokinesDisease Models, AnimalImmunohistochemistryInflammation MediatorsLipopolysaccharidesMaleMAP Kinase Signaling SystemMiceNF-kappa BSemaphorin-3ASignal TransductionCytokinesInflammation MediatorsLipopolysaccharidesNF-kappa BSemaphorin-3AApoptosisInflammationJNKLipopolysaccharideRac1Semaphorin-3a

Identifiers

PMID29909462
OpenAlexW2808369043

What OpenQuestion holds

Textmetadata
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.