Evidence map›Paper›PMID 40223052›Full record

ArticleRespiratory research2025

MFGE8 regulates the EndoMT of HLMECs through the BMP signaling pathway and fibrosis in acute lung injury.

Qingqiang Shi, Huang Liu, Hanghang Wang, Ling Tang, Qi Di, Daoxin Wang

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Article in Respiratory research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

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5citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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5 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Qingqiang ShiThe Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Huang LiuThe Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Hanghang WangThe Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Ling TangThe Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Qi DiThe Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Daoxin WangThe Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. wangdaoxin0163@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTo investigate the effects and mechanisms of MFGE8 on LPS-induced endothelial-to-mesenchymal transition (EndoMT) and pulmonary fibrosis in human lung microvascular endothelial cells (HLMECs) and a mouse model of acute lung injury.

methodsSerum MFGE8 levels were compared between ARDS patients and controls. In vitro, HLMECs were treated with LPS, siRNA targeting MFGE8, and recombinant human MFGE8 (rhMFGE8).HLMEC morphology, invasion, migration, and EndoMT markers (CD31, ɑ-SMA) were evaluated. BMP/Smad1/5-Smad4 signaling and Snail expression were assessed via immunofluorescence, western blotting, and qRT-PCR. In vivo, rhMFGE8 effects on pulmonary fibrosis and EndoMT were analyzed in a mouse model of acute lung injury.

resultsMFGE8 levels were significantly reduced in ARDS patients, with higher levels correlating to better survival. In vitro, rhMFGE8 improved HLMEC morphology, reduced invasion and migration, and attenuated LPS-induced EndoMT by increasing CD31 and decreasing α-SMA. MFGE8 knockdown increased BMP/Smad1/5-Smad4 signaling and Snail expression, while rhMFGE8 inhibited these effects. In vivo, rhMFGE8 ameliorated pulmonary fibrosis and EndoMT in mice.

conclusionsMFGE8 regulates LPS-induced EndoMT in HLMECs via the BMP/Smad1/5-Smad4 pathway and protects against pulmonary fibrosis in acute lung injury, suggesting it as a therapeutic target for ALI and ARDS.

Indexed as

Acute Lung InjuryBone Morphogenetic ProteinsEndothelial CellsEpithelial-Mesenchymal TransitionLungPulmonary FibrosisAnimalsCells, CulturedDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLMiddle AgedSignal TransductionBone Morphogenetic ProteinsAcute lung injuryEndothelial-to-mesenchymal transitionHuman lung microvascular endothelial cellsMilk fat globule factor 8Smad1/5/Smad4

Identifiers

PMID40223052
PMCPMC11995649

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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.