Reducing Endogenous Labile Zn May Help to Reduce Smooth Muscle Cell Injury around Vascular Stents

Abstract

Vascular stent service involves complex service environments and performance requirements, among which the histocompatibility of the stent could seriously affect the therapeutic effect. In the pathology of vascular disease, the thin fiber cap is easily ruptured, exposing the necrotic core below, and triggering a series of dangerous biochemical reactions. In contrast, the thin neointima, considered an essential structure growing on the stent, may evolve into vulnerable plaque structures due to lesions induced by the stent. Therefore, the reduction of necrosis around the stent below the thin neointima is indispensable. In this work, different cell model experiments suggested that the content of endogenous labile Zn positively correlated with cell injury. Zinquin-Zn fluorescence experiments and zinc ion channels research suggested that the change in the content of endogenous labile Zn in smooth muscle cells is affected by different stent coatings. The content of endogenous labile Zn in cells negatively correlated with cell viability. Animal experiments indirectly verified the increase in endogenous labile Zn by detecting the expression of Zn regulatory protein (metallothionein) in the necrotic tissues. Reducing the content of endogenous labile Zn may favor a reduction in smooth muscle cell injury and necrosis. This biochemical mechanism is effective in improving the therapeutic effect of vascular stents.

Advances in Nanoparticles in the Prevention and Treatment of Myocardial Infarction

“…MI includes ST-segment Elevation Myocardial Infarction (STEMI) and Non-ST-Segment Elevation Myocardial infarction (NSTEMI) [ 12 ]. STEMI is caused by the exposure of the necrotic core after the rupture of the coronary lipid plaque, which induces the formation of an acute occlusive thrombus and ischemia of the entire myocardial layer, resulting in ST-segment elevation [ 13 ]. Compared with STEMI, NSTEMI mainly induces acute non-occlusive thrombosis on the basis of coronary plaque injury, or occlusive thrombosis with good collateral circulation, which manifests as ST-segment depression on an electrocardiogram [ 14 ].…”