» Articles » PMID: 36891137

Extracellular Vesicles and Duchenne Muscular Dystrophy Pathology: Modulators of Disease Progression

Overview
Journal Front Physiol
Date 2023 Mar 9
PMID 36891137
Authors
Affiliations
Soon will be listed here.
Abstract

Duchenne muscular dystrophy (DMD) is a devastating disorder and is considered to be one of the worst forms of inherited muscular dystrophies. DMD occurs as a result of mutations in the dystrophin gene, leading to progressive muscle fiber degradation and weakness. Although DMD pathology has been studied for many years, there are aspects of disease pathogenesis and progression that have not been thoroughly explored yet. The underlying issue with this is that the development of further effective therapies becomes stalled. It is becoming more evident that extracellular vesicles (EVs) may contribute to DMD pathology. EVs are vesicles secreted by cells that exert a multitude of effects their lipid, protein, and RNA cargo. EV cargo (especially microRNAs) is also said to be a good biomarker for identifying the status of specific pathological processes that occur in dystrophic muscle, such as fibrosis, degeneration, inflammation, adipogenic degeneration, and dilated cardiomyopathy. On the other hand, EVs are becoming more prominent vehicles for custom-engineered cargos. In this review, we will discuss the possible contribution of EVs to DMD pathology, their potential use as biomarkers, and the therapeutic efficacy of both, EV secretion inhibition and custom-engineered cargo delivery.

Citing Articles

Isolation of small extracellular vesicles from regenerating muscle tissue using tangential flow filtration and size exclusion chromatography.

Gurriaran-Rodriguez U, De Repentigny Y, Kothary R, Rudnicki M Skelet Muscle. 2024; 14(1):22.

PMID: 39394606 PMC: 11468478. DOI: 10.1186/s13395-024-00355-1.


Caveolin and NOS in the Development of Muscular Dystrophy.

Nakashima M, Suga N, Yoshikawa S, Matsuda S Int J Mol Sci. 2024; 25(16).

PMID: 39201459 PMC: 11354531. DOI: 10.3390/ijms25168771.


Molecular regulation of myocyte fusion.

Wherley T, Thomas S, Millay D, Saunders T, Roy S Curr Top Dev Biol. 2024; 158:53-82.

PMID: 38670716 PMC: 11503471. DOI: 10.1016/bs.ctdb.2024.01.016.


Challenges and Considerations of Preclinical Development for iPSC-Based Myogenic Cell Therapy.

Sun C, Serra C, Kalicharan B, Harding J, Rao M Cells. 2024; 13(7.

PMID: 38607035 PMC: 11011706. DOI: 10.3390/cells13070596.


Generalizable anchor aptamer strategy for loading nucleic acid therapeutics on exosomes.

Han G, Zhang Y, Zhong L, Wang B, Qiu S, Song J EMBO Mol Med. 2024; 16(4):1027-1045.

PMID: 38448545 PMC: 11018858. DOI: 10.1038/s44321-024-00049-7.


References
1.
Sampaolesi M, Blot S, DAntona G, Granger N, Tonlorenzi R, Innocenzi A . Mesoangioblast stem cells ameliorate muscle function in dystrophic dogs. Nature. 2006; 444(7119):574-9. DOI: 10.1038/nature05282. View

2.
Crewe C, Funcke J, Li S, Joffin N, Gliniak C, Ghaben A . Extracellular vesicle-based interorgan transport of mitochondria from energetically stressed adipocytes. Cell Metab. 2021; 33(9):1853-1868.e11. PMC: 8429176. DOI: 10.1016/j.cmet.2021.08.002. View

3.
Skog J, Wurdinger T, van Rijn S, Meijer D, Gainche L, Sena-Esteves M . Glioblastoma microvesicles transport RNA and proteins that promote tumour growth and provide diagnostic biomarkers. Nat Cell Biol. 2008; 10(12):1470-6. PMC: 3423894. DOI: 10.1038/ncb1800. View

4.
Yao S, Chen Z, Yu Y, Zhang N, Jiang H, Zhang G . Current Pharmacological Strategies for Duchenne Muscular Dystrophy. Front Cell Dev Biol. 2021; 9:689533. PMC: 8417245. DOI: 10.3389/fcell.2021.689533. View

5.
Messina E, De Angelis L, Frati G, Morrone S, Chimenti S, Fiordaliso F . Isolation and expansion of adult cardiac stem cells from human and murine heart. Circ Res. 2004; 95(9):911-21. DOI: 10.1161/01.RES.0000147315.71699.51. View