Evidence map›Paper›PMID 36059026›Full record

ArticleJournal of translational medicine2022

Lumican is elevated in the lung in human and experimental acute respiratory distress syndrome and promotes early fibrotic responses to lung injury.

Ke Wang, Youyu Wang, Yufang Cao, Hao Wang, Yongfang Zhou, Lijuan Gao, Zijian Zeng, Mengxin Cheng, Xiaodong Jin, Jun Chen and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 29 citations in OpenAlex.

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  20. Role of Interleukin-6 Family Cytokines in Organ Fibrosis.Kidney diseases (Basel, Switzerland) · 2023
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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

12 authors at 3 institutions in 1 country.

Ke Wang *Division of Pulmonary Diseases, State Key Laboratory of Biotherapy, and Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, No. 37, Guoxue Alley, Chengdu, 610041, Sichuan, China.
Youyu Wang *Department of Thoracic Surgery, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, China.
Yufang Cao *Department of Critical Care Medicine, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, China.
Hao Wang *Division of Pulmonary Diseases, State Key Laboratory of Biotherapy, and Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, No. 37, Guoxue Alley, Chengdu, 610041, Sichuan, China.
Yongfang ZhouDepartment of Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, China.
Lijuan GaoDivision of Pulmonary Diseases, State Key Laboratory of Biotherapy, and Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, No. 37, Guoxue Alley, Chengdu, 610041, Sichuan, China.
Zijian ZengDivision of Pulmonary Diseases, State Key Laboratory of Biotherapy, and Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, No. 37, Guoxue Alley, Chengdu, 610041, Sichuan, China.
Mengxin ChengDivision of Pulmonary Diseases, State Key Laboratory of Biotherapy, and Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, No. 37, Guoxue Alley, Chengdu, 610041, Sichuan, China.
Xiaodong JinDepartment of Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, China.
Jun ChenDivision of Pulmonary Diseases, State Key Laboratory of Biotherapy, and Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, No. 37, Guoxue Alley, Chengdu, 610041, Sichuan, China.
Fuqiang WenDivision of Pulmonary Diseases, State Key Laboratory of Biotherapy, and Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, No. 37, Guoxue Alley, Chengdu, 610041, Sichuan, China. wenfuqiang@scu.edu.cn.ORCID 0000-0001-6205-4758
Tao WangDivision of Pulmonary Diseases, State Key Laboratory of Biotherapy, and Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, No. 37, Guoxue Alley, Chengdu, 610041, Sichuan, China. tao.wang@scu.edu.cn.
Sichuan University · CNCentral South University · CNSichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFibroproliferative repair starts early in the inflammatory phase of acute respiratory distress syndrome (ARDS) and indicates a poor prognosis. Lumican, a small leucine-rich proteoglycan, is implicated in homeostasis and fibrogenesis, but its role in ARDS is unclear.

methodsBronchoalveolar lavage fluid (BALF) samples were obtained from ARDS patients (n = 55) enrolled within 24 h of diagnosis and mechanically ventilated (n = 20) and spontaneously breathing (n = 29) control subjects. Lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse models were intratracheally administered an adeno-associated virus (AAV) vector expressing lumican shRNA. Primary human lung fibroblasts (HLF) and small airway epithelial cells (SAECs) were cultured with tumour necrosis factor (TNF)-α or lumican. Luminex/ELISA, histochemistry/immunohistochemistry, immunofluorescence microscopy, quantitative real-time PCR, and western blotting were performed.

resultsLumican levels were significantly higher in the BALF of ARDS patients than in that of ventilated or spontaneously breathing controls (both p < 0.0001); they were correlated with the PaO

conclusionsPulmonary lumican levels were increased early in human and experimental ARDS and linked to disease severity and inflammatory fibrotic processes. Lumican triggers the transdifferentiation of lung fibroblasts into myofibroblasts and epithelial-mesenchymal transition in SAECs, possibly via the ERK/Slug pathway. Knockdown of pulmonary lumican attenuated extracellular matrix deposition in ALI mice. Overall, lumican promotes fibrotic responses in the early phase of ARDS, suggesting its potential as a therapeutic target.

Indexed as

Acute Lung InjuryRespiratory Distress SyndromeAnimalsBronchoalveolar Lavage FluidCytokinesDisease Models, AnimalFibronectinsFibrosisHumansLipopolysaccharidesLumicanLungMiceTumor Necrosis Factor-alphaCytokinesFibronectinsLipopolysaccharidesLumicanTumor Necrosis Factor-alphaAcute respiratory distress syndromeEarly phaseInflammationLumicanLung injuryProfibrotic response

Identifiers

PMID36059026
PMCPMC9440861
OpenAlexW4294670063

What OpenQuestion holds

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Registered trials

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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.