Effect of Activated Protein Kinase C Beta Type Mediated Phosphorylation of Signal Transducer and Activator of Transcription 4 on Proliferation and Phenotypic Transformation of Vascular Smooth Muscle Cells After Vascular Injury Induced by Nano-SiO₂.

The excessive proliferation, endothelial migration, and phenotype transformation of vascular smooth muscle cells (VSMC) lead to increased extracellular matrix secretion, which induces vascular intimal hyperplasia, which is an important restenosis mechanism after vascular injury. In our study, we verified the cytotoxicity of SiO₂ nanoparticles to VSMC. To explore the role of endothelial repairs and molecular mechanisms after vascular injuries, we sequenced the transcriptome of injured vessels in the carotid artery of mice.