Evidence map›Paper›PMID 40616692›Full record

ArticleLung2025

Cmpk2 Protects Against Acute Lung Injury in Mice.

Lei Zhao, Ling Lei, Jiashi Guo, Ling Meng, Huan Zhang, Zhenting He, Sijia Fan, Ziling Deng, Qinke He, Cuihong Wang and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Lung, 2025. 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

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

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.

Lei ZhaoSchool of Basic Medical Sciences & Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400042, China.
Ling LeiSchool of Basic Medical Sciences & Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400042, China.
Jiashi GuoSchool of Basic Medical Sciences & Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400042, China.
Ling MengSchool of Basic Medical Sciences & Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400042, China.
Huan ZhangSchool of Basic Medical Sciences & Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400042, China.
Zhenting HeSchool of Basic Medical Sciences & Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400042, China.
Sijia FanSchool of Basic Medical Sciences & Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400042, China.
Ziling DengSchool of Basic Medical Sciences & Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400042, China.
Qinke HeSchool of Basic Medical Sciences & Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400042, China.
Cuihong WangSchool of Basic Medical Sciences & Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400042, China.
Yiming XiangSchool of Basic Medical Sciences & Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400042, China.
Jingjing QinSchool of Basic Medical Sciences & Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400042, China.
Shuliang GuoDepartment of Pulmonary and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400042, China. GUOSL999@sina.com.
Chunguang RenSchool of Basic Medical Sciences & Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400042, China. chunguangren@cqmu.edu.cn.

Funding

Key Project of Chongqing Technological Innovation and Application Development Special Project CSTC2021jscx-gksb-N0028National Natural Science Foundation of China 32170766National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai NRCTM(SH)-2025-08
6 · The paper itself

Abstract

purposeAcute respiratory distress syndrome (ARDS)/Acute lung injury (ALI), characterized by severe hypoxemia and pulmonary edema, involves mitochondrial dysfunction. Cytidine/uridine monophosphate kinase 2 (Cmpk2), a mitochondrial metabolic enzyme, modulates inflammation and senescence, yet its role in ARDS remains unclear. We investigated Cmpk2's function in Pseudomonas aeruginosa (P. aeruginosa)-induced ALI using Cmpk2 global knockout (KO) mice.

methodsCmpk2 was identified through mitochondrial gene expression analysis of ARDS datasets (GEO). Murine ALI was induced by intratracheal P. aeruginosa injection. Lung pathology (hematoxylin and eosin staining), leukocyte recruitment (flow cytometry), and cytokines (ELISA) were assessed. GO/KEGG analyses were conducted to identify Cmpk2-associated biological processes and pathways. The expression of Cmpk2 in leukocyte populations was analyzed using single-cell RNA sequencing (scRNA-seq) data from ARDS patient samples. Mouse neutrophils' phagocytosis of P. aeruginosa was quantified by flow cytometry. Zebrafish embryos were infected with P. aeruginosa and Staphylococcus aureus for bacterial burden and survival assays.

resultsCmpk2 expression was significantly upregulated in ARDS. Cmpk2 KO exacerbated P. aeruginosa-induced ALI in mice, as evidenced by increased pathological damage and permeability, elevated proinflammatory cytokines and enhanced neutrophil infiltration. GO/KEGG analyses linked Cmpk2 to innate immunity. scRNA-seq analysis revealed an enriched expression of Cmpk2 in neutrophils. Cmpk2 deficiency impaired neutrophil phagocytosis and reduced host survival during bacterial infection, accomplished by decreased STING expression. The differences in phagocytosis between the wild-type and Cmpk2 KO mouse neutrophils/zebrafish embryos were eliminated by STING inhibitor C176.

conclusionCmpk2 protects against pneumonia by attenuating neutrophil recruitment and enhancing bacterial phagocytosis via STNG-dependent mechanisms.

Indexed as

Acute Lung InjuryPseudomonas InfectionsRespiratory Distress SyndromeAnimalsCytokinesDisease Models, AnimalHumansLungMiceMice, Inbred C57BLMice, KnockoutNeutrophilsPhagocytosisPseudomonas aeruginosaZebrafishCytokinesAcute lung injuryCmpk2NeutrophilPhagocytosisRecruitment

Identifiers

PMID40616692

What Socratic holds

Textmetadata
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 Socratic graph.