Review highlights cellular mechanisms behind neointimal hyperplasia in hemodialysis access, suggesting targeted interventions and bioengineering solutions.
Recurrent stenosis in hemodialysis access remains a critical challenge.Recent evidence suggests that access failure is better understood as a remodeling imbalance between adaptive outward expansion and maladaptive inward narrowing.This review highlights key mechanisms driving this imbalance, including hemodynamic shear stress sensors (Sox17, OPN/CD44) and epigenetic regulation (METTL3).We propose a therapeutic paradigm shift: moving beyond nonspecific suppression of cell growth toward targeted molecular interventions that restore the remodeling balance and biological restoration using self-healing tissue-engineered grafts.
No takes yet. Share an insight, caveat, or question.
Lee et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: