Evidence map›Paper›PMID 42401819›Full record

ArticleMolecular medicine (Cambridge, Mass.)2026

Dopamine signaling reprograms macrophage FAO to alleviate acute lung injury by inhibiting NETosis via the CXCL10-CXCR3 axis.

Ximing Liao, Changwen Deng, Jing Gao, Ziqi Yang, Tian Li, Jialin Yao, Muyun Wang, Fengyang Xie, Zhaoqi Li, Kun Wang and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Ximing Liao *Department of Pulmonary and Critical Care Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Changwen Deng *Department of Pulmonary and Critical Care Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Jing Gao *Department of Pulmonary and Critical Care Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Ziqi Yang *Department of Pulmonary and Critical Care Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Tian LiDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Jialin YaoDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Muyun WangDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Fengyang XieDepartment of General Practice, Shanghai Jing'an District Caojiadu Community Health Center, Shanghai, 200040, China.
Zhaoqi LiSchool of Medicine, Saint George's University, True blue GGD 000, West Indies, Grenada.
Kun WangDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Qiang LiDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China. liqressh1962@163.com.
Di WuDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China. windcreator_wudi@126.com.
Wujian XuDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China. wujian_xu@163.com.
Wei GaoDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China. grace19881118@126.com.ORCID http://orcid.org/0000-0003-1026-3878

Funding

Healthcare Talents Youth Program of Shanghai Pudong New Area 2025PDWSYCQN-02National Natural Science Foundation of China 82270116National Natural Science Foundation of China 82470073National Natural Science Foundation of China 82502637National Natural Science Foundation of China 82570119Natural Science Foundation of Shanghai Municipality 25ZR1402443Shanghai Science and Technology Development Foundation 24QA2707100Young Scientists Research Fund of Shanghai East Hospital DFPY2025011
6 · The paper itself

Abstract

backgroundDysregulated innate immunity and oxidative stress drive the pathogenesis of acute lung injury/acute respiratory distress syndrome (ALI/ARDS), yet master endogenous regulators that orchestrate inflammation resolution remain elusive.

methodsThis study employed public database mining, clinical data investigation, murine disease models, mouse bone marrow-derived macrophages and neutrophils, and human macrophages from healthy donors and ARDS patients, to investigate the dynamic changes of the dopaminergic signaling system in the acute pulmonary inflammatory environment and its role in regulating macrophage metabolism and neutrophil extracellular trap formation (NETosis).

resultsPublic database mining and experimental data reveal accelerated dopamine (DA) turnover during ALI. DA, signaling via D1-like receptors, reprograms macrophage metabolism by enhancing carnitine palmitoyltransferase 1 A (CPT1A)-dependent fatty acid oxidation (FAO) and mitochondrial fitness, which is coupled with the suppression of MAPK/NF-κB and NLRP3 inflammasome activation. These modulated macrophages restrain neutrophilic inflammation by secreting IL-10 to inhibit the CXCL10-CXCR3 axis, thereby curtailing neutrophil hyperactivation and pathogenic NETosis. Crucially, this protective mechanism is conserved in human macrophages from both healthy donors and ARDS patients.

conclusionOur findings establish DA as a therapeutic target for recalibrating innate immunity in ALI, providing a mechanistically grounded framework for targeting dopaminergic signaling to resolve dysregulated inflammation, with exploratory preclinical translational implications for ALI/ARDS therapy.

Indexed as

Acute Lung InjuryChemokine CXCL10DopamineExtracellular TrapsFatty AcidsMacrophagesReceptors, CXCR3Signal TransductionAnimalsDisease Models, AnimalHumansMaleMiceNeutrophilsOxidation-ReductionChemokine CXCL10DopamineFatty AcidsReceptors, CXCR3Acute lung injuryDopamineMacrophage metabolismMitochondrial homeostasisNeutrophil extracellular traps

Identifiers

PMID42401819
PMCPMC13617839

What OpenQuestion holds

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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.