Therapeutic Potential of Exosomes in Pulmonary Fibrosis

Pulmonary fibrosis is closely associated with the recruitment of fibroblasts from capillary vessels with damaged endothelial cells, the epithelial mesenchymal transition (EMT) of type II alveolar epithelial cells, and the transformation of fibroblasts to myofibroblasts. Recent studies suggest that E...

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Bibliographic Details
Published inFrontiers in pharmacology Vol. 11; p. 590972
Main Authors Xie, Linshen, Zeng, Ye
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 04.12.2020
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Summary:Pulmonary fibrosis is closely associated with the recruitment of fibroblasts from capillary vessels with damaged endothelial cells, the epithelial mesenchymal transition (EMT) of type II alveolar epithelial cells, and the transformation of fibroblasts to myofibroblasts. Recent studies suggest that EMT is a key factor in the pathogenesis of pulmonary fibrosis, as the disruption of EMT-related effector molecules can inhibit the occurrence and development of PF. With the numerous advancements made in molecular biology in recent years, researchers have discovered that exosomes and their cargos, such as miRNAs, lncRNAs, and proteins, can promote or inhibit the EMT, modulate the transformation of fibroblasts into myofibroblasts, contribute to the proliferation of fibroblasts and promote immunoregulatory and mitochondrial damage during pulmonary fibrosis. Exosomes are key factors regulating the differentiation of bone marrow mesenchymal stem cells (BMSCs) into myofibroblasts. Interestingly, exosomes derived from BMSCs under pathological and physiological conditions may promote or inhibit the EMT of type II alveolar epithelial cells and the transformation of fibroblasts into myofibroblasts to regulate pulmonary fibrosis. Thus, exosomes may become a new direction in the study of drugs for the treatment of pulmonary fibrosis.
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Edited by: Raffaele Strippoli, Sapienza University of Rome, Italy
Reviewed by: Alice Conigliaro, University of Palermo, Italy
Inmaculada Navarro-Lérida, Spanish National Centre for Cardiovascular Research, Spain
This article was submitted to Inflammation Pharmacology, a section of the journal Frontiers in Pharmacology
ISSN:1663-9812
1663-9812
DOI:10.3389/fphar.2020.590972