Atherosclerosis Treatment with Stimuli-Responsive Nanoagents: Recent Advances and Future Perspectives.

Atherosclerosis is the root of approximately one-third of global mortalities. Nanotechnology exhibits splendid prospects to combat atherosclerosis at the molecular level by engineering smart nanoagents with versatile functionalizations. Significant advances in nanoengineering enable nanoagents to autonomously navigate in the bloodstream, escape from biological barriers, and assemble with their nanocohort at the targeted lesion. The assembly of nanoagents with endogenous and exogenous stimuli breaks down their shells, facilitates intracellular delivery, releases their cargo to kill the corrupt cells, and gives imaging reports. All these improvements pave the way toward personalized medicine for atherosclerosis. This review systematically summarizes the recent advances in stimuli-responsive nanoagents for atherosclerosis management and its progress in clinical trials.

Progress and prospects of endothelial progenitor cell therapy in coronary stent implantation.

Drug-eluting stents (DES) have been widely used to treat coronary artery disease (CAD) since their clinical use has significantly reduced the occurrence of in-stent restenosis (ISR) as compared with the initially applied bare-metal stents (BMS). However, analyses of long-term clinical outcome have raised concerns about the serious safety problem of DES, such as ISR caused by late or very late thrombosis. Various studies showed that those complications were associated with vascular endothelial injury/dysfunction or endothelialization delaying. Recently, through biological characterization of endothelial progenitor cells (EPCs), mechanistic understanding of rapid re-endothelialization of the vascular injury sites after coronary stenting has become possible and is a new research hotspot in the prevention of ISR and late/very late stent thrombosis. It has been well recognized that the formation of a functional endothelial layer from EPCs requires a coordinated sequence of multistep and signaling events, which includes cell mobilization, adhesion, migration and finally the differentiation to vascular endothelial cells (VECs). In this review, we summarize and discuss the currently relevant information about EPCs, the mechanism of DES interfering with the natural vascular healing process in preventing or delaying the formation of a functional endothelial layer, and EPCs-mediated acceleration of re-endothelialization at vascular injury sites. © 2015 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 104B: 1237-1247, 2016.

Id1: a novel therapeutic target for patients with atherosclerotic plaque rupture.

Plaque neovascularization and inflammation are responsible for plaque destabilization and rupture. However, the precise triggers for inflammation and neovascularization in atherosclerosis are largely unknown. Id1 (inhibitor of DNA-binding) protein is a helix-loop-helix transcription factor and plays an important role in angiogenesis and inflammation. The expression of Id1 can be up-regulated by plaque formation factors such as vascular endothelial growth factor (VEGF), hypoxia, NAD(P)H oxidase, and TNF-alpha. Moreover, Id1 is critical to endothelial progenitor cell (EPC) population formation and angiogenesis. Evidence from diverse sources has suggested that Id1 may affect plaque destabilization through angiogenesis and inflammation. Herein we hypothesize that Id1 is an important protein for the development and progression of atherosclerotic plaque destabilization and hence blocking the expression of Id1 may serve as new targets for antiatherogenic therapy.