CCN5 suppresses injury-induced vascular restenosis by inhibiting smooth muscle cell proliferation and facilitating endothelial repair via thymosin β4 and Cd9 pathway
Authors' conclusion
CCN5 exerts a dual protective effect on ISR by inhibiting VSMC proliferation and facilitating EC repair.
Study context
- Population
- In-stent restenosis (ISR) patients; stent-implanted porcine coronary arteries; injured mouse femoral arteries
Main finding
As reported in the abstract
- Plasma CCN5 significantly reduced and closely correlated with degree of restenosis in ISR patients
- CCN5 expression decreased in vascular smooth muscle cell (VSMCs) of stented porcine coronary segments and injured mouse femoral arteries, especially synthetic VSMCs; elevated in regenerating endothelial cell (ECs)
- EC- and VSMC-specific CCN5 deletion exacerbated injury-induced neointimal hyperplasia; CCN5 gain-of-function alleviated neointimal formation
- Tβ4 identified as CCN5 interacting protein in ECs; EC-CCN5 promoted injury repair via Tβ4 cleavage product Ac-SDKP
- CCN5rp promoted EC repair to suppress neointimal hyperplasia via interaction with Cd9 extracellular domain
- CCN5rp-coated stent significantly increased strut coverage with ECs, suppressed neointimal formation and alleviated ISR (porcine model)
Original publication
CCN5 suppresses injury-induced vascular restenosis by inhibiting smooth muscle cell proliferation and facilitating endothelial repair via thymosin β4 and Cd9 pathway. Eur Heart J. Published 28 January 2025. doi:10.
Summarised from the published abstract; every number is checked against it