Evidence map›Paper›PMID 29950923›Full record

ReviewMediators of inflammation2018

The Role of Macrophages in the Pathogenesis of ALI/ARDS.

Xiaofang Huang, Huiqing Xiu, Shufang Zhang, Gensheng Zhang

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05101694 (Study on the Correlation Between Alveolar Macrophage-derived Autophagosomes and the Severity of Lung Injury in ARDS), which is not on this map. Cited by 232 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
232citing papers in PubMed, 2 pooled it
13.4field-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.

NCT05101694 unknown statusnot on this mapstarted 2022, after this paper: background citation

Study on the Correlation Between Alveolar Macrophage-derived Autophagosomes and the Severity of Lung Injury in ARDS

Typeobservational_patient_registrySponsorSoutheast University, ChinaRan2022 to 2023Enrolled60ConditionsARDS
3 · Its place in the literature

Who cites it

232 citing papers in PubMed, 2 syntheses or guidelines pooled it, 393 citations in OpenAlex.

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  15. Disulfidptosis modification patterns are involved in the immune microenvironment regulation of septic acute respiratory distress syndrome.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026
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172 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Xiaofang HuangDepartment of Critical Care Medicine, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, China.
Huiqing XiuDepartment of Critical Care Medicine, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, China.
Shufang ZhangDepartment of Cardiology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, China.
Gensheng ZhangDepartment of Critical Care Medicine, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, China.ORCID 0000-0001-9298-3961
Second Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite development in the understanding of the pathogenesis of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), the underlying mechanism still needs to be elucidated. Apart from leukocytes and endothelial cells, macrophages are also essential for the process of the inflammatory response in ALI/ARDS. Notably, macrophages play a dual role of proinflammation and anti-inflammation based on the microenvironment in different pathological stages. In the acute phase of ALI/ARDS, resident alveolar macrophages, typically expressing the alternatively activated phenotype (M2), shift into the classically activated phenotype (M1) and release various potent proinflammatory mediators. In the later phase, the M1 phenotype of activated resident and recruited macrophages shifts back to the M2 phenotype for eliminating apoptotic cells and participating in fibrosis. In this review, we summarize the main subsets of macrophages and the associated signaling pathways in three different pathological phases of ALI/ARDS. According to the current literature, regulating the function of macrophages and monocytes might be a promising therapeutic strategy against ALI/ARDS.

Indexed as

Acute Lung InjuryAnimalsHumansMacrophagesMacrophages, AlveolarRespiratory Distress Syndrome

Identifiers

PMID29950923
PMCPMC5989173
OpenAlexW2802595885

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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.