MSCs/EVs-based therapy targeting DAD: research progress and future perspectives from ARDS and COVID-19 to RP-ILD.

ingentiumby ingentium

In Discovery Literature.

Publication date: Jun 15, 2026

Diffuse alveolar damage (DAD) is the core pathological process of acute lung injury, characterized by dual injury to alveolar epithelial and capillary endothelial cells, initiation of an inflammatory storm, and subsequent fibrotic remodeling, with persistently high clinical mortality. This pathological change is not restricted to a single disease but widely exists in critical pulmonary disorders such as acute respiratory distress syndrome (ARDS), severe COVID-19, and rapidly progressive interstitial lung disease (RP-ILD), acting as a key driver of disease progression. In recent years, mesenchymal stromal cells (MSCs) and their derived extracellular vesicles (EVs) have become research hotspots for their superior immunomodulatory, anti-apoptotic, tissue-repair, and anti-fibrotic properties. Based on the DAD pathological framework, this article systematically correlates epithelial barrier injury, inflammatory cascade amplification and pulmonary fibrotic remodeling with the therapeutic mechanisms of MSCs and their derived EVs in ARDS, COVID-19 and RP-ILD. It aims to provide a solid basis for the clinical translation of MSCs- and EVs-based therapies and promote their development into a mechanism-driven therapeutic paradigm targeting DAD, with great clinical value and academic innovation.

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Concepts Keywords
Academic Coronavirus disease 2019
Dad Diffuse alveolar damage
Immunomodulatory Extracellular vesicles
Pulmonary Immunomodulation
Remodeling Tissue repair

Semantics

Type Source Name
disease MESH COVID-19
disease MESH acute lung injury
disease MESH injury
disease MESH acute respiratory distress syndrome
disease MESH interstitial lung disease
disease MESH disease progression
pathway REACTOME Translation
pathway REACTOME Reproduction
disease MESH included
disease MESH inflammation
disease MESH aberrant tissue
disease MESH lung injury
disease MESH hypoxemia
disease MESH critically ill
disease MESH long COVID
disease MESH myositis
disease MESH melanoma
pathway KEGG Melanoma
disease MESH dermatomyositis
disease MESH secondary infection
disease MESH fibrosis
disease MESH pneumonia
disease MESH AEC
disease MESH pulmonary edema
disease MESH edema
disease MESH atelectasis
disease MESH thrombosis
disease MESH Necrosis
disease MESH traps
pathway REACTOME Defensins
pathway REACTOME Apoptosis
disease MESH pulmonary fibrosis
drug DRUGBANK Coenzyme M
pathway REACTOME Budding
drug DRUGBANK Tretamine
drug DRUGBANK Dinoprostone
disease MESH death
pathway KEGG Ferroptosis
drug DRUGBANK Glutathione
disease MESH iron overload
disease MESH HGF
pathway REACTOME Release
drug DRUGBANK Isoxaflutole
pathway KEGG Tight junction
disease MESH LPS
disease MESH burns
drug DRUGBANK N-acetylsulfanilyl chloride
disease MESH CBP
drug DRUGBANK Methionine
disease MESH strains
drug DRUGBANK Methylprednisolone
drug DRUGBANK Cyclophosphamide
drug DRUGBANK Tacrolimus
disease MESH MSC+EV
disease MESH tumor
disease MESH pathological processes
disease MESH NOD
disease MESH Arthritis
disease MESH Dis
disease MESH Rmd
disease MESH coronavirus infection
drug DRUGBANK Mesenchymal Stem Cells
drug DRUGBANK Diethylstilbestrol
disease MESH Des
disease MESH connective tissue disease

Original Article

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