Fibrotic remodeling and tissue regeneration mechanisms define the therapeutic potential of human muscular progenitors

Fibrosis is an intrinsic biological reaction toward the challenges of tissue injury that is implicated in the wound‐healing process. Although it is useful to efficiently mitigate the damage, progression of fibrosis is responsible for the morbidity and mortality occurring in a variety of diseases. Be...

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Veröffentlicht in:Bioengineering & translational medicine 2023-03, Vol.8 (2), p.e10439-n/a
Hauptverfasser: Hsiao, Ya‐Chuan, Wang, I‐Han, Yang, Tsung‐Lin
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Sprache:eng
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Zusammenfassung:Fibrosis is an intrinsic biological reaction toward the challenges of tissue injury that is implicated in the wound‐healing process. Although it is useful to efficiently mitigate the damage, progression of fibrosis is responsible for the morbidity and mortality occurring in a variety of diseases. Because of lacking effective treatments, there is an emerging need for exploring antifibrotic strategies. Cell therapy based on stem/progenitor cells is regarded as a promising approach for treating fibrotic diseases. Appropriate selection of cellular sources is required for beneficial results. Muscle precursor cells (MPCs) are specialized progenitors harvested from skeletal muscle for conducting muscle regeneration. Whether they are also effective in regulating fibrosis has seldom been explored and merits further investigation. MPCs were successfully harvested from all human samples regardless of demographic backgrounds. The extracellular matrices remodeling was enhanced through the paracrine effects mediated by MPCs. The suppression effects on fibrosis were confirmed in vivo when MPCs were transplanted into the diseased animals with oral submucous fibrosis. The data shown here revealed the potential of MPCs to be employed to simultaneously regulate both processes of fibrosis and tissue regeneration, supporting them as the promising cell candidates for development of the cell therapy for antifibrosis and tissue regeneration.
ISSN:2380-6761
2380-6761
DOI:10.1002/btm2.10439