Intimal hyperplasia (IH) results from excessive vascular smooth muscle cell (VSMC) proliferation, migration through the internal elastic lamina, and extracellular matrix (ECM) protein deposition, orchestrated by various physical and molecular factors in the vasculature. IH is a common complication following endovascular treatments or angioplasty procedures and remains poorly managed despite decades of research. Although many molecular factors contributing to IH have been identified over recent years, earlier studies have not fully integrated these discoveries. Recent research has largely concentrated on VSMC proliferation, migration, and dedifferentiation. This review aims to comprehensively elucidate the molecular pathways involved in all stages of IH development, including endothelial injury, the coagulation cascade, inflammation, ECM deposition, and vascular remodeling, to inform future therapeutic strategies. We extensively searched PubMed for relevant animal studies reporting molecular mechanism involved in formation of IH and included 56 articles. In total, we found 69 molecules and 6 pathways involved in all stages of IH. Among the molecular pathways involved, the Mitogen-activated Protein Kinase (MAPK), Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB), and Transforming Growth Factor Beta (TGF-β).pathways consistently emerge in almost each step of IH development. This highlights the need for a multifaceted and comprehensive treatment to prevent IH.
Indriani et al. (Fri,) studied this question.