Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Vascular restenosis, a pathological recurrence of lumen narrowing following interventions, remains a major limitation to the long-term success of vascular procedures. Its development is centrally driven by neointimal hyperplasia, a process orchestrated by endothelial injury, phenotypic switching of vascular smooth muscle cells (VSMCs) from a contractile to a synthetic state, and a coordinated inflammatory response. Despite advancements, the molecular mechanisms are not fully elucidated, and specific, effective pharmacotherapies are still lacking. This review systematically delineates the pathophysiology, focusing on these three core elements, and provides a comprehensive landscape of the complex signaling networks and molecular targets. We extensively cover protein-based regulators-including pro-proliferative factors (e.g., LSD1, FGF10), protective mediators (e.g., CGRP, A20), dual-action molecules with isoform-specific or context-dependent effects (e.g., KLFs, HDACs), endothelial repair targets (e.g., VEGF), and molecules that coordinately target both VSMCs and endothelial cells (ECs) (e.g., PERK, METTL3). We place significant focus on non-coding RNAs, particularly microRNAs (miRNAs) like miR-221/222, which fine-tune multiple targets in both VSMCs and ECs, offering unique precision. We critically evaluate the therapeutic significance and clinical translation potential, while a

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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