Evidence map›Paper›PMID 35103290›Full record

ArticleMolecular medicine reports2022

Overexpression of Foxc1 ameliorates sepsis‑associated encephalopathy by inhibiting microglial migration and neuroinflammation through the IκBα/NF‑κB pathway.

Hongyu Wang, Hongwei Wang, Yinsen Song, Congyan Liu, Xinling Qian, Dalong Zhang, Xin Jiang, Sisen Zhang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Transcriptomics and metabolomics reveal the protective effect of β-hydroxybutyrate on sepsis associated encephalopathy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  4. Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy.International journal of molecular sciences · 2026
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  14. p65 enhanced METTL3-mediated mCentral-European journal of immunology · 2025
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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

8 authors at 5 institutions in 1 country.

Hongyu WangDepartment of Critical Care Medicine, The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong 510280, P.R. China.
Hongwei WangDepartment of Respiratory Medicine, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200092, P.R. China.
Yinsen SongDepartment of Emergency Medicine, People's Hospital of Henan University of Chinese Medicine/Zhengzhou People's Hospital, Zhengzhou, Henan 450003, P.R. China.
Congyan LiuDepartment of Critical Care Medicine, The Fifth Clinical Medical College of Henan University of Chinese Medicine, Zhengzhou, Henan 450003, P.R. China.
Xinling QianDepartment of Emergency Medicine, People's Hospital of Henan University of Chinese Medicine/Zhengzhou People's Hospital, Zhengzhou, Henan 450003, P.R. China.
Dalong ZhangDepartment of Emergency Medicine, People's Hospital of Henan University of Chinese Medicine/Zhengzhou People's Hospital, Zhengzhou, Henan 450003, P.R. China.
Xin JiangDepartment of Emergency Medicine, People's Hospital of Henan University of Chinese Medicine/Zhengzhou People's Hospital, Zhengzhou, Henan 450003, P.R. China.
Sisen ZhangDepartment of Critical Care Medicine, The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong 510280, P.R. China.
Zhengzhou People's Hospital · CNFirst Affiliated Hospital of Henan University · CNShanghai Jiao Tong University · CNSouthern Medical University · CNXinHua Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis‑associated encephalopathy (SAE) is a common and severe complication of sepsis. The cognitive dysfunction that ensues during SAE has been reported to be caused by impairments of the hippocampus. Microglia serves a key role in neuroinflammation during SAE through migration. Forkhead box C1 (Foxc1) is a member of the forkhead transcription factor family that has been found to regulate in cell migration. However, the role of Foxc1 in neuroinflammation during SAE remains unknown. In the present study, the mechanistic role of Foxc1 on microglial migration, neuroinflammation and neuronal apoptosis during the occurrence of cognitive dysfunction in SAE was investigated. A microglia‑mediated inflammation model was induced by LPS in BV‑2 microglial cells

Indexed as

Cognitive DysfunctionSepsis-Associated EncephalopathyAnimalsMiceMice, Inbred C57BLMicrogliaNeuroinflammatory DiseasesNF-kappa BNF-KappaB Inhibitor alphaNF-kappa BNF-KappaB Inhibitor alphaforkhead box C1IκBα/NF‑κB pathwaymicrogliamigrationneuroinflammationsepsis‑associated encephalopathy

Identifiers

PMID35103290
PMCPMC8822881
OpenAlexW4210708234

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.