Evidence map›Paper›PMID 35752760›Full record

ArticleMolecular medicine (Cambridge, Mass.)2022

ISM1 suppresses LPS-induced acute lung injury and post-injury lung fibrosis in mice.

Ngan Nguyen, Simin Xu, Terence Yin Weng Lam, Wupeng Liao, W S Fred Wong, Ruowen Ge

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
10.8field-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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Mechanism of Action ofBiology · 2026
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  18. Rodent Models of Lung Disease: A Road Map for Translational Research.International journal of molecular sciences · 2025
    Review
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  20. 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

6 authors at 1 institution in 1 country.

Ngan NguyenDepartment of Biological Sciences, Faculty of Science, National University of Singapore, Singapore, 117543, Republic of Singapore.
Simin XuDepartment of Biological Sciences, Faculty of Science, National University of Singapore, Singapore, 117543, Republic of Singapore.
Terence Yin Weng LamDepartment of Biological Sciences, Faculty of Science, National University of Singapore, Singapore, 117543, Republic of Singapore.
Wupeng LiaoDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 117600, Republic of Singapore.
W S Fred WongDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 117600, Republic of Singapore.
Ruowen GeDepartment of Biological Sciences, Faculty of Science, National University of Singapore, Singapore, 117543, Republic of Singapore. dbsgerw@nus.edu.sg.ORCID 0000-0002-0750-7336
National University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute lung injury/acute respiratory distress syndrome (ALI/ARDS) are clinical syndromes characterized by acute lung inflammation, pulmonary edema and hypoxemia, with up to 50% mortality rate without effective pharmacological therapy. Following the acute inflammation, repair and remodeling occurs which in some cases resulting in lung fibrosis. The pathophysiology of ALI/ARDS remains incompletely understood. Lipopolysaccharide (LPS)-induced ALI in mice have been widely used as a model to study human ALI/ARDS. Isthmin 1 (ISM1) is a secreted protein highly abundant in mouse lung. We have previously reported that upon intratracheal LPS instillation, ISM1 expression in the lung is further upregulated. Recently, we also reported that ISM1 is an anti-inflammatory protein in the lung with Ism1

methodsUsing Ism1

resultsWe reveal that ISM1 deficiency in mice led to an intensified acute lung inflammation upon intratracheal LPS challenge, with a heightened leukocyte infiltration including neutrophils and monocyte-derived alveolar macrophages, as well as upregulation of multiple pro-inflammatory cytokines/chemokines including tumor necrosis factor α (TNF-α). Although innate immune cells largely subsided to the baseline by day 7 post-LPS challenge in both wild-type and Ism1

conclusionTogether with our previous report, this work further established ISM1 as an endogenous anti-inflammation protein in the lung, restraining excessive host inflammatory response to LPS-triggered ALI and suppressing post-ALI lung fibrosis likely through suppressing NF-κB activation and pro-inflammatory cytokine/chemokine production.

Indexed as

Acute Lung InjuryPneumoniaPulmonary FibrosisRespiratory Distress SyndromeAnimalsAnti-Inflammatory AgentsCytokinesIntercellular Signaling Peptides and ProteinsLipopolysaccharidesLungMiceNF-kappa BAnti-Inflammatory AgentsCytokinesIntercellular Signaling Peptides and Proteinsisthmin protein, mouseLipopolysaccharidesNF-kappa BAcute lung injuryInflammationISM1LPSPulmonary fibrosis

Identifiers

PMID35752760
PMCPMC9233842
OpenAlexW4283447161

What OpenQuestion holds

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LicenceCC BY
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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.