Oxidized lipids and systemic inflammatory biomarkers, such as an elevated C-reactive protein to albumin ratio (HR 1.13), serve as critical mechanistic mediators and clinical predictors for carotid in-stent restenosis.
Carotid artery stenting (CAS) has emerged as an effective alternative to carotid endarterectomy for treating carotid artery stenosis, particularly in high-risk surgical patients. However, in-stent restenosis (ISR) remains a significant complication, occurring in 10–30% of patients within the first year after CAS and substantially impacting long-term clinical outcomes. The pathophysiology of ISR involves complex molecular cascades, with oxidative stress and lipid peroxidation playing pivotal roles in neointimal hyperplasia and vascular remodeling. This review provides a comprehensive analysis of oxidized lipids in carotid ISR, focusing on their molecular mechanisms of action and potential as clinical biomarkers. We examine the biochemical pathways leading to lipid oxidation following stent implantation, dissect the molecular mechanisms through which oxidized lipids promote vascular pathology, and evaluate emerging therapeutic strategies. Understanding oxidized lipid pathophysiology offers opportunities for improved risk stratification and targeted therapeutic interventions. Future research should focus on validating specific oxidized lipid biomarkers and developing therapeutic strategies targeting oxidized lipid pathways to prevent ISR and improve patient outcomes following carotid artery stenting.
Chen et al. (Mon,) conducted a review in Carotid in-stent restenosis. Oxidized lipids and systemic inflammatory biomarkers, such as an elevated C-reactive protein to albumin ratio (HR 1.13), serve as critical mechanistic mediators and clinical predictors for carotid in-stent restenosis.