Urolithin B suppresses phenotypic switch in vascular smooth muscle cells induced by PDGF-BB via inhibiting the PI3K-AKT pathway.

Atherosclerosis (AS) is a prevalent cardiovascular condition, and the growth and phenotypic switch of vascular smooth muscle cells (VSMCs) play a crucial role in its development. Studies have revealed that the activation of certain transcription factors and signaling pathways can trigger these cellular changes. Consequently, targeting these pathways and pivotal molecules has emerged as a promising strategy for AS treatment. Drugs that can reverse the cellular changes in VSMCs may offer new therapeutic options for AS, marking a significant advancement. While previous research has suggested that urolithin B (Uro B) possesses anti-atherosclerotic properties, its exact mechanism remains to be fully understood, especially the effect of Uro B in VSMCs. This study discovered that Uro B can impede the proliferation and migration of VSMCs prompted by PDGF-BB, as well as their phenotypic changes, indicating that Uro B could potentially prevent AS by inhibiting the phenotypic switch of VSMCs.