ArticleActa neuropathologica communications2026
Angiotensin II impairs the remyelination mediated by brain endothelial cell-derived exosomes.
Article in Acta neuropathologica communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
White matter hyperintensities (WMH), characterized by myelin loss and axonal injury, are largely driven by hypertension, their most significant modifiable risk factor. The role of endothelial cell-derived exosomes (EC-Exos) in oligodendrocyte precursor cell (OPCs)-mediated remyelination within WMH remains critical but poorly defined. This study investigated the function of EC-Exos in remyelination by comparing exosomes from angiotensin II-treated brain microvascular endothelial cells (AngII-Exos; modeling hypertensive conditions) with those from untreated cells (BMEC-Exos; modeling normotensive conditions). In vitro, BMEC-Exos promoted OPCs differentiation, evidenced by increased myelin basic protein (MBP) expression and reduced immature NG2+ OPCs. AngII-Exos lost this pro-differentiation capacity, instead suppressing OPCs proliferation and inducing immature OPCs accumulation. In vivo, the focal demyelination mouse model showed that BMEC-Exos injected into the lateral ventricle migrated to lesions, enhancing MBP intensity and reducing NG2+ areas, while AngII-Exos failed to promote remyelination. Lipidomic analysis revealed AngII-Exos exhibited altered fatty acid profiles, including reduced levels of essential myelin-related lipids (e.g., FFA 18:1, 22:0) and elevated FFA 22:6, impairing their ability to supply lipid precursors for OPCs maturation. These findings demonstrate that Ang II disrupts EC-Exos lipid composition, compromising their pro-remyelination effects on OPCs, which may represent a critical pathological mechanism underlying hypertension-associated white matter damage. This study provides new mechanistic insights into vascular contributions to myelin repair and pathology.
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