In individuals with coronary artery disease (CAD) and peripheral artery disease (PAD), vascular restenosis is still a substantial issue (PAD). A key underlying disease is neointimal hyperplasia, which is characterised by post-procedure proliferation and migration of vascular smooth muscle cells (VSMCs). Interleukin 11 (IL-11) was examined in a mouse model of injury-related plaque formation. Apoe/ mice were fed a hyperlipidemic diet and had their right carotid wire injured. Anti-IL11 antibody (X203), IgG control antibody, or buffer were administered into mice. We used ultrasound to determine the thickness of the vessel wall and the rate of blood flow. When compared to control, X203 treatment reduced post-endothelial injury vessel wall thickness and injury-related plaque in mice with carotid wire injury. In compared to the control, immunofluorescence staining of the injury-related plaque revealed that X203 therapy reduced the number of VSMCs, lowered matrix metalloproteinase 2 (MMP2) levels, and decreased collagen content. In comparison to control, X203 therapy was linked with a considerable increase in smooth muscle protein 22 (SM22) positive cells in injury-related plaque, implying that the contractile VSMC phenotype was preserved. In contrast to IgG, X203 lowered the collagen content of undamaged carotid arteries, indicating that hyperlipidemia-induced arterial remodelling can occur even in the absence of mechanical injury.
