Table 7 Summary of studies on the role of extracellular vesicles in lung fibrosis.

BMSC-Exos

Lung macrophage

Hyperoxia-induced BPD

Suppress M1 macrophage production and enhance M2 macrophage generation

Improve lung function, decrease fibrosis and pulmonary vascular remodeling, and ameliorate pulmonary hypertension.

[144]

hBMSC-Exos

Lung macrophage

Bleomycin-induced pulmonary fibrosis

Regulate total lung imbalance of macrophage phenotype

Prevent or reverse lung fibrosis

[145]

UC-MSC-Exos

PAEC and PASMC

Monocrotaline-induced rat model of PH

Regulate Wnt5a/BMP signaling pathway

Attenuate pulmonary vascular remodeling and lung fibrosis

[146]

UC-MSC-Exos

Lung tissue

BPD

Immunomodulatory glycoprotein TSG-6

Improve pulmonary inflammation, pulmonary simplification, pulmonary hypertension, and right ventricular hypertrophy

[147]

BMSC-EVs

IPF pulmonary tissue

IPF

MiR‐29b‐3p

Ameliorate IPF

[148]

BMSC-EVs

Lung fibroblast

PF

MiR-186 suppressed SOX4 and DKK1 expression, blocked fibroblast activation

Ameliorate IPF

[149]

hPMSC -EVs

Lung fibroblast

Whole thorax irradiation mouse model

MiR-214-3p downregulate ATM/P53/P21 signaling

Relieve radiation-induced lung inflammation and fibrosis

[150]

MenSCs-Exos

Recipient alveolar epithelial cells

BLM

MiRNA Let-7 suppresses ROS, mtDNA damage, and NLRP3 inflammasome activation

Remit pulmonary fibrosis

[151]

MSC-Exos

MLE-12 cells^*

LPS-induced ALI

Transmit miR-23a-3p and miR-182-5p to inhibit NF-κB and hedgehog pathways

Reversed the LPS-induced lung injury and fibrosis

[152]