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. 2025 Apr 16;14(8):600. doi: 10.3390/cells14080600

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© 2025 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Molecular mechanisms responsible for MSC-EVs-dependent recovery of injured dopaminergic neurons. MSC-EVs easily bypass the BBB and deliver various neurotrophic and immunosuppressive factors to injured dopaminergic neurons, enhancing their viability and function. Additionally, MSC-EVs attenuate microglia-driven inflammatory responses and prevent inflammation-induced injury of dopaminergic neurons. By delivering IL-10 and TGF-β, MSC-EVs suppress the production of inflammatory cytokines (TNF-α and IL-6) in microglia and increase the production of dopamine, 5-hydroxytryptamine (5-HT) and their metabolites (3,4-Dihydroxyphenyl acetic acid (DOPAC), and homovanillic acid (HVA)) in injured dopaminergic neurons. Additionally, MSC-EVs-sourced Gli-1 prevents apoptosis of dopaminergic neurons by suppressing the activation of specificity protein 1 (SP-1), which enhances the expression of the pro-apoptotic Bax gene. Additionally, by activating SMAD3 and p38/MAPK signaling pathways in brain endothelial cells, MSC-EVs facilitates the growth of vascular networks, which improves blood flow to injured dopaminergic neurons, improving their survival and viability.