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Review
. 2023 Apr 4:2023:4245704.
doi: 10.1155/2023/4245704. eCollection 2023.

Mesenchymal Stem Cell-derived Exosomes: Novel Therapeutic Approach for Inflammatory Bowel Diseases

Affiliations
Review

Mesenchymal Stem Cell-derived Exosomes: Novel Therapeutic Approach for Inflammatory Bowel Diseases

Cheng-Mei Tian et al. Stem Cells Int. .

Abstract

As double membrane-encapsulated nanovesicles (30-150 nm), exosomes (Exos) shuttle between different cells to mediate intercellular communication and transport active cargoes of paracrine factors. The anti-inflammatory and immunomodulatory activities of mesenchymal stem cell (MSC)-derived Exos (MSC-Exos) provide a rationale for novel cell-free therapies for inflammatory bowel disease (IBD). Growing evidence has shown that MSC-Exos can be a potential candidate for treating IBD. In the present review, we summarized the most critical advances in the properties of MSC-Exos, provided the research progress of MSC-Exos in treating IBD, and discussed the molecular mechanisms underlying these effects. Collectively, MSC-Exos had great potential for cell-free therapy in IBD. However, further studies are required to understand the full dimensions of the complex Exo system and how to optimize its effects.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Biogenesis, composition, and uptake pathway of exosomes. (a) Exosomes were derived from the endosomal pathway. Extracellular biomaterial enters the cytoplasm through endocytosis pathway, then fuses with early endosome and develops into late endosome. Then, forms intraluminal vesicles (ILVs) containing vesicle structure in MVBs. When MVB fuses with lysosomes, it degrades the contents. When MVBs were transferred to plasma membrane resulting in the release of exosomes into the extracellular space. Endosomal sorting complex (ESCRT)-independent and dependent pathways required for exosome transport are involved in various stages of exosome formation. (b) Exosome components include proteins, lipids, nucleic acids, and small molecules, as well as surface proteins. (c) Exosomes can exert their effects by binding to receptors present on the surface of target cells, or through endocytosis, membrane fusion, macrophage.
Figure 2
Figure 2
The effects of MSC-EVs on immune effector cells in IBD.
Figure 3
Figure 3
Schematic representation of IBD treatment using MSC-derived exosomes.

References

    1. Ng S. C., Shi H. Y., Hamidi N., et al. Worldwide incidence and prevalence of inflammatory bowel disease in the 21st century: a systematic review of population-based studies. The Lancet . 2017;390(10114):2769–2778. doi: 10.1016/S0140-6736(17)32448-0. - DOI - PubMed
    1. Imhann F., Vich Vila A., Bonder M. J., et al. Interplay of host genetics and gut microbiota underlying the onset and clinical presentation of inflammatory bowel disease. Gut . 2018;67(1):108–119. doi: 10.1136/gutjnl-2016-312135. - DOI - PMC - PubMed
    1. McGovern D. P., Kugathasan S., Cho J. H. Genetics of Inflammatory bowel diseases. Gastroenterology . 2015;149(5):1163–1176.e2. doi: 10.1053/j.gastro.2015.08.001. - DOI - PMC - PubMed
    1. Ramos G. P., Papadakis K. A. Mechanisms of disease: inflammatory bowel diseases. Mayo Clinic Proceedings . 2019;94(1):155–165. doi: 10.1016/j.mayocp.2018.09.013. - DOI - PMC - PubMed
    1. Shouval D. S., Rufo P. A. The role of environmental factors in the pathogenesis of inflammatory bowel Diseases. JAMA Pediatrics . 2017;171(10):999–1005. doi: 10.1001/jamapediatrics.2017.2571. - DOI - PubMed