Evidence map›Paper›PMID 33141376›Full record

ArticleInflammation2021

Mechanisms of Renal-Splenic Axis Involvement in Acute Kidney Injury Mediated by the α7nAChR-NF-κB Signaling Pathway.

Yang Gao, Kai Kang, Yan-Song Liu, Na-Na Li, Qiu-Yuan Han, Hai-Tao Liu, Wei-Lan Kong, Xing Zhang, Rui Huang, Zhen-Yu Yang and 10 more

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 40% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Dexmedetomidine and acute kidney injury in patients with sepsis: a retrospective cohort study.Canadian journal of anaesthesia = Journal canadien d'anesthesie · 2025
    Article
  3. Review
  4. 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

20 authors at 1 institution in 1 country.

Yang Gao *Department of Critical Care Medicine, The First Affiliated Hospital of Harbin Medical University, No.23 Youzheng Street, Harbin, 150001, China.
Kai Kang *Department of Critical Care Medicine, The First Affiliated Hospital of Harbin Medical University, No.23 Youzheng Street, Harbin, 150001, China.
Yan-Song LiuDepartment of Critical Care Medicine, The Harbin Medical University Cancer Hospital, Harbin, 150081, China.
Na-Na LiDepartment of Critical Care Medicine, The First Affiliated Hospital of Harbin Medical University, No.23 Youzheng Street, Harbin, 150001, China.
Qiu-Yuan HanDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Hai-Tao LiuDepartment of Critical Care Medicine, The Harbin Medical University Cancer Hospital, Harbin, 150081, China.
Wei-Lan KongDepartment of Critical Care Medicine, The First Affiliated Hospital of Harbin Medical University, No.23 Youzheng Street, Harbin, 150001, China.
Xing ZhangDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Rui HuangDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Zhen-Yu YangDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Zhi-Dong QiDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Jun-Bo ZhengDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Ming LiDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Hong-Liang WangDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Jia-Yu LiDepartment of Critical Care Medicine, The Harbin Medical University Cancer Hospital, Harbin, 150081, China.
Rui-Jin LiuDepartment of Critical Care Medicine, The Harbin Medical University Cancer Hospital, Harbin, 150081, China.
Si-Cong WangDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Wei-Hua Zhang *Department of Pathophysiology, Harbin Medical University, 157 Baojian Road, Harbin, 150081, China. zhangwh116@126.com.
Ming-Yan Zhao *Department of Critical Care Medicine, The First Affiliated Hospital of Harbin Medical University, No.23 Youzheng Street, Harbin, 150001, China. mingyan0927@126.com.
Kai-Jiang Yu *Department of Critical Care Medicine, The First Affiliated Hospital of Harbin Medical University, No.23 Youzheng Street, Harbin, 150001, China. drkaijiang1@126.com.ORCID http://orcid.org/0000-0002-8429-6616
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to investigate the effect of splenectomy on dexmedetomidine-activated cholinergic anti-inflammatory pathway-mediated alleviation of LPS-induced AKI. A mouse model of septic kidney injury was established in C57BL/6 mice. A total of 30 C57BL/6 mice were randomly divided into the control group, LPS group, dexmedetomidine + LPS group, splenectomy group, splenectomy + LPS group, and splenectomy + dexmedetomidine + LPS group. The pathological effects in kidney tissues in each group were analyzed by HE staining. Apoptosis in each group was examined by the TUNEL method. Cr and Cys-C levels in each group were measured by ELISA. The expression levels of IL-6, NF-κB p65, Caspase-3, the antiapoptotic protein Bcl-2, the proapoptotic protein Bax, and α7nAChR in each group were measured by qRT-PCR and Western blotting. Dexmedetomidine alone reduced apoptosis in kidney tissue; however, apoptosis was increased after splenectomy in mice treated with dexmedetomidine. Splenectomy reduced the production of proinflammatory cytokines in circulation and had a protective effect on the kidney. Splenectomy inhibited dexmedetomidine-mediated activation of the α7nAChR pathway. Dexmedetomidine effectively alleviated LPS-induced kidney injury, and splenectomy inhibited the anti-inflammatory, antiapoptotic, and renoprotective effects of dexmedetomidine. The kidney-spleen axis is mediated by the α7nAChR-NF-κB signaling pathway and is involved in the development of AKI.

Indexed as

Acute Kidney Injuryalpha7 Nicotinic Acetylcholine ReceptorAnimalsAnti-Inflammatory AgentsApoptosisBiomarkersBlotting, WesternDexmedetomidineEnzyme-Linked Immunosorbent AssayIn Situ Nick-End LabelingKidneyLipopolysaccharidesMaleMiceMice, Inbred C57BLNF-kappa Balpha7 Nicotinic Acetylcholine ReceptorAnti-Inflammatory AgentsBiomarkersDexmedetomidineLipopolysaccharidesNF-kappa BAKIapoptosischolinergic anti-inflammatory pathwaydexmedetomidineinflammatory reactionsplenectomyα7nAChR

Identifiers

PMID33141376
OpenAlexW3096593981

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.