Evidence map›Paper›PMID 41569334›Full record

ArticleCellular and molecular life sciences : CMLS2026

HUVEC-derived exosomes alleviate lipopolysaccharide-induced acute lung injury inflammation by restoring the balance of mitochondrial fusion and division.

Wei Lai, Songhela Ahan, Zhang Ying, Wanli Jiang

Abstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
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

4 authors.

Wei LaiDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Songhela AhanDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Zhang YingDepartment of Vascular Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, 430060, China.
Wanli JiangDepartment of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan, 430060, China. RM003262@whu.edu.cn.ORCID http://orcid.org/0009-0002-7389-9638

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSepsis is a life-threatening condition with high morbidity and mortality, where acute lung injury (ALI) is one of the earliest and most severe complications. Macrophage-mediated overactivation of inflammation and subsequent release of pro-inflammatory cytokines cause significant damage to pulmonary epithelial cells, playing a critical role in the progression of sepsis-induced ALI. This study successfully investigated the role of HUVEC-derived exosomes in the treatment of ALI and designed a novel engineered vesicle for therapeutic application.

resultsWe successfully isolated and characterized HUVEC-derived exosomes. These exosomes were found to reduce inflammatory cytokine release from macrophages and restore the viability of lung epithelial cells. Furthermore, extracellular vesicles derived from HUVECs effectively suppress proinflammatory cytokine release from M1-polarized macrophages. Significantly, HUVEC-derived exosomes improved the balance between mitochondrial fusion and fission, reducing the release of mitochondrial DNA (mtDNA) and nuclear translocation of NF-κB. miRNA profiling and subsequent inhibition experiments identified miR-520d-3p as a key factor delivered by HUVEC exosomes. This miRNA was shown to decrease the expression of MARCH5, inhibiting ubiquitination of the mitochondrial fusion protein Mfn1, thus promoting mitochondrial fusion and reducing mtDNA release. In addition, we designed and synthesized a novel engineered vesicle, exosome@IPR, by encapsulating ipratropium bromide within HUVEC-derived exosomes to target mitochondrial fusion. This engineered vesicle significantly reduced lung injury and improved the survival rate in mice.

conclusionOur findings uncover a novel therapeutic mechanism by which miR-520d-3p delivered via HUVEC-derived exosomes alleviates inflammation in sepsis-induced ALI. This occurs through modulation of mitochondrial dynamics, specifically by restoring the balance between mitochondrial fusion and fission, thereby mitigating macrophage-induced lung injury in sepsis. Our findings revealed that extracellular vesicles derived from HUVECs act as a natural therapeutic agent by restoring the balance between mitochondrial fusion and fission. Building on this, we designed and synthesized an engineered vesicle named exosome@IPR that more effectively reverses the LPS-induced imbalance in mitochondrial dynamics, reduces inflammation, and improves survival in mice.

Indexed as

Acute Lung InjuryExosomesHuman Umbilical Vein Endothelial CellsInflammationMitochondrial DynamicsAnimalsCytokinesDNA, MitochondrialHumansLipopolysaccharidesMacrophagesMaleMiceMice, Inbred C57BLMicroRNAsMitochondriaCytokinesDNA, MitochondrialLipopolysaccharidesMicroRNAsAcute lung injuryExosome@IPRLiposomeMitochondriaNew delivery

Identifiers

PMID41569334
PMCPMC12876537

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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.