Biomaterials Promote the Regression of Atherosclerotic Plaque by Regulating Cell Behavior

Atherosclerosis is characterized by the deposition of lipid within arterial walls, precipitating the initiation and progression of atherosclerotic lesions. Over time, these plaques enlarge and rupture, initiating thrombosis cascades that pose significant risks to patient safety. Conventional therapies, including 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (eg, statins) and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, predominantly target lipid reduction while overlooking the intricate microenvironment within atherosclerotic plaque. Statins possess limited lipid-lowering efficacy and may even exhibit insensitivity or intolerance in patients. While PCSK9 inhibitors, as adjuvant therapy, demonstrate potent lipid-lowering effects, they fail to further stabilize vulnerable plaques. In contrast, biomaterials have emerged as pivotal tools for addressing unstable plaques. By restoring endothelial cell (EC) function, inhibiting neutrophil activation, modulating macrophage behavior, and preventing the phenotypic transformation of smooth muscle cells, biomaterials effectively promote plaque regression. This review explores the pathogenesis of atherosclerosis and highlights recent advancements in biomaterial-based therapies for vulnerable plaques, aiming to offer novel insights and solutions to this pressing global health challenge.