Factors Modulating Mitochondrial Function after Arterial Injury: Past-to-Present Evidence for the Devising of Future Preventive and Therapeutic Strategies.

Vascular trauma can lead to adverse outcomes if remodeling is uncontrolled. Intimal hyperplasia (IH) is a key process that contributes to luminal narrowing during remodeling and is strongly influenced by mitochondria. Enhanced mitochondrial ATP production and increased production of reactive oxygen species (ROS), along with reduced apoptosis in vascular smooth muscle cells (VSMCs), have been shown to promote IH. In addition, endothelial injury could initiate mitochondrial dysfunction and apoptosis which compromise endothelial integrity and function, leading to the exposure of VSMCs to various circulating factors, thus triggering IH. Therefore, reduction of mitochondrial ATP production, reduction of ROS, and induction of apoptosis in VSMC after vascular injury may present promising strategies in preventing IH. Conversely, promoting re-endothelialization prevents exposure of VSMCs to blood circulation. This review provides comprehensive insights from in vitro and in vivo reports of potential therapeutic strategies attempt to alleviate IH and achieve optimal outcomes.