ArticleJournal of translational medicine2026
3D-Mesenchymal stromal cells derived VASH2 alleviates oxidative stress-induced endothelial senescence by mediating α-tubulin detyrosination in systemic sclerosis.
Article in Journal of translational medicine, 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
backgroundEndothelial cell (EC) senescence driven by oxidative stress is a pivotal contributor to vasculopathy in systemic sclerosis (SSc), leading to impaired angiogenesis and loss of vascular integrity. Three-dimensional (3D) cultured human umbilical cord-derived mesenchymal stromal cells (MSCs) represent a promising therapeutic strategy for SSc due to their enhanced anti-fibrotic and immunomodulatory properties. However, their potential to mitigate EC senescence remains unclear. This study aims to investigate whether 3D-MSCs confer superior therapeutic effects over conventional MSCs by ameliorating EC senescence and to elucidate the underlying mechanism.
methodsThe anti-senescent effects of 3D-MSCs and two-dimensional (2D)-MSCs were compared in vitro using a hydrogen peroxide (H₂O₂)-induced EC senescence model and in vivo using a bleomycin-induced SSc mouse model. RNA sequencing identified vasohibin-2 (VASH2) as a key factor, which was further validated using siRNA knockdown. The specific inhibitor EpoY was used to assess the role of VASH2 in microtubule detyrosination in senescent ECs.
results3D-MSCs prevented H₂O₂-induced EC senescence and restored angiogenic capacity in vitro. Administration of 3D-MSCs ameliorated skin fibrosis and vasculopathy in SSc mouse models by mitigating EC senescence, thereby improving vascular density and restoring endothelial barrier integrity. Mechanistically, 3D-MSCs secreted VASH2, which then interacted with the small vasohibin-binding protein (SVBP) to restore microtubule detyrosination in senescent ECs under oxidative stress. Inhibition of the VASH/SVBP complex by EpoY impaired the anti-senescent benefits of 3D-MSCs.
conclusionsOur study demonstrates that 3D-MSCs alleviate oxidative stress-induced EC senescence and associated vasculopathy primarily via VASH2 secretion, which restores α-tubulin detyrosination to promote microtubule stability. These findings reveal a novel mechanism against EC senescence and underscore the therapeutic potential of 3D-MSCs in vasculopathy.
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