Evidence map›Paper›PMID 37003346›Full record

ArticleBiochemical pharmacology2023

Lyn attenuates sepsis-associated acute kidney injury by inhibition of phospho-STAT3 and apoptosis.

Nannan Li, Guoxin Lin, Hao Zhang, Jian Sun, Ming Gui, Yan Liu, Wei Li, Zishun Zhan, Yisu Li, Shiqi Pan and 2 more

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Biochemical pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Research progress on animal models of contrast-induced acute kidney injury.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Nannan LiDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha 410013, China. Electronic address: 208311024@csu.edu.cn.
Guoxin LinDepartment of Anesthesiology, The Third Xiangya Hospital, Central South University, Changsha 410013, China. Electronic address: lgx_mzk@csu.edu.cn.
Hao ZhangDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha 410013, China. Electronic address: zhanghaoliaoqing@163.com.
Jian SunDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha 410013, China. Electronic address: sunjian105@sina.com.
Ming GuiDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha 410013, China. Electronic address: zkbgm@126.com.
Yan LiuDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha 410013, China. Electronic address: nianbiecabell@sina.com.
Wei LiDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha 410013, China. Electronic address: liweiss2008@126.com.
Zishun ZhanDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha 410013, China. Electronic address: zzs414656@163.com.
Yisu LiDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha 410013, China. Electronic address: 1334868LYS@163.com.
Shiqi PanDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha 410013, China. Electronic address: psq202056831@163.com.
Jishi LiuDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha 410013, China. Electronic address: csuljs@163.com.
Juan TangDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha 410013, China. Electronic address: 603123@csu.edu.cn.
Central South University · CNThird Xiangya Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis-associated acute kidney injury (SA-AKI) is a life-threatening condition associated with high mortality and morbidity. However, the underlying pathogenesis of SA-AKI is still unclear. Lyn belongs to Src family kinases (SFKs), which exert numerous biological functions including modulation in receptor-mediated intracellular signaling and intercellular communication. Previous studies demonstrated that Lyn gene deletion obviously aggravates LPS-induced lung inflammation, but the role and possible mechanism of Lyn in SA-AKI have not been reported yet. Here, we found that Lyn protected against renal tubular injury in cecal ligation and puncture (CLP) induced AKI mouse model by inhibition of signal transducer and activator of transcription 3 (STAT3) phosphorylation and cell apoptosis. Moreover, Lyn agonist MLR-1023 pretreatment improved renal function, inhibited STAT3 phosphorylation and decreased cell apoptosis. Thus, Lyn appears to play a crucial role in orchestrating STAT3-mediated inflammation and cell apoptosis in SA-AKI. Hence, Lyn kinase may be a promising therapeutic target for SA-AKI.

Indexed as

Acute Kidney InjurySepsisAnimalsApoptosisKidneyMiceSTAT3 Transcription FactorSTAT3 Transcription FactorApoptosisInflammationLynSA-AKISTAT3

Identifiers

PMID37003346
OpenAlexW4361249623

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.