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.
Lee et al. (Mon,) studied this question.