Evidence map›Paper›PMID 36497185›Full record

ArticleCells2022

Nrf2 Deficiency Exacerbated CLP-Induced Pulmonary Injury and Inflammation through Autophagy- and NF-κB/PPARγ-Mediated Macrophage Polarization.

Jing Luo, Jin Wang, Jing Zhang, Aming Sang, Xujun Ye, Zhenshun Cheng, Xinyi Li

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
12.8field-weighted citation impact, top 1% 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

57 citing papers in PubMed, 98 citations in OpenAlex.

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  9. CYP1B1 modulates stress and repair pathways in airway cells challenged by wood smoke particles.Toxicological sciences : an official journal of the Society of Toxicology · 2026
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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

7 authors at 2 institutions in 1 country.

Jing LuoDepartment of Anesthesiology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Jin WangDepartment of Anesthesiology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Jing ZhangDepartment of Anesthesiology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Aming SangDepartment of Anesthesiology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Xujun YeDepartment of Geriatrics, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Zhenshun ChengDepartment of Respiratory and Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Xinyi LiDepartment of Anesthesiology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Wuhan University · CNZhongnan Hospital of Wuhan University · CN

Funding

Climbing Project for Medical Talent of Zhongnan Hospital No.PDJH202205Hubei Provincial Natural Science Foundation No.2020CFB199National Natural Science Foundation of China No.82002033
6 · The paper itself

Abstract

The balance between M1 and M2 macrophage polarization is involved in the regulation of pulmonary inflammation. Nuclear factor erythroid-derived 2-like 2 (Nfe2l2, also known as Nrf2), a nuclear transcription factor, is reported to play protective roles in acute lung injury (ALI) and inflammation, and increasing evidence indicates that the protective effects of Nrf2 are closely related to autophagy. This study aimed to explore whether Nrf2 is involved in sepsis-induced acute pulmonary injury and inflammation and in the role of macrophage polarization in the process. In the present study, sepsis patients, an Nrf2 knockout mouse that underwent cecal ligation and puncture (CLP), and lipopolysaccharide (LPS)-treated macrophage cell lines were employed to investigate the potential functions of Nrf2 in sepsis-induced lung injury and the underlying mechanisms. Clinical studies showed that the NRF2 mRNA level was inversely correlated with pulmonary inflammation and disease severity in patients with sepsis. Analyses in a CLP-treated Nrf2 knockout mouse model indicated that an Nrf2 deficiency promoted a CLP-induced increase in M1 macrophage polarization and apoptosis and inhibited CLP-induced upregulation of the autophagy level in lung tissues. Experiments in RAW264.7 cells revealed that Nrf2 overexpression inhibited M1 macrophage polarization but promoted M2 macrophage polarization by improving the autophagy, and Nrf2 overexpression promoted PPARγ but inhibited NF-κB nuclear translocation. In conclusion, these results indicate that Nrf2 plays a protective role in sepsis-induced pulmonary injury and inflammation through the regulation of autophagy- and NF-κB/PPARγ-mediated macrophage polarization.

Indexed as

Acute Lung InjuryMacrophagesSepsisAnimalsAutophagyInflammationMiceMice, KnockoutNF-E2-Related Factor 2NF-kappa BPPAR gammaNfe2l2 protein, mouseNF-E2-Related Factor 2NF-kappa BPPAR gammaacute lung injuryautophagymacrophage polarizationNrf2pulmonary inflammation

Identifiers

PMID36497185
PMCPMC9735993
OpenAlexW4310682250

What OpenQuestion holds

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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 OpenQuestion graph.