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    • In accordance with our study the blockage of Fas

    2022-06-30

    In accordance with our study, the blockage of Fas/FasL pathway and overexpression of miR-204-5p was associated with reduced BUN, Scr, and MDA, as well as elevated SOD and GSH-Px. A recent study has reported the ectopic expression of BUN and Scr in RIRI animals, which marked the dysfunction of kidney associated with internal damage [24], and this is in concert with the findings of the present study. Besides, it is well documented that MDA, the end-product of lipid peroxidation, was known as the most critical mechanism of RIRI [25]. SOD is generally regarded as a natural hedge against oxidative injury, and the potential role of induction or administration of SOD in limiting RIRI and/or oxidative stress has been previously proposed [26]. According to a prior study, MDA and GSH-Px, as the endogenous antioxidants, were improved by FDP-Sr, while the Fas/FasL pathway was down-regulated [27]. Besides, another study revealed that downregulated Fas and FasL could decrease Scr and BUN levels to suppress RIRI in rats [10]. Furthermore, it has been previously demonstrated that miR-204 could reduce the ectopic BUN in Candidemia mice [28]. The findings of this study suggested that restored miR-204-5p or decreased Fas and FasL reduced BUN, Scr, and MDA but boosted SOD and GSH-Px, thus alleviating RIRI.
    Materials and methods
    Authors’ contributions
    Conflicts of interest
    Acknowledgments
    Introduction Coronary artery disease (CAD) is the major cause of morbidity and mortality in western countries [1]. CAD is mainly caused by atherosclerosis, which is narrowing and hardening of capreomycin receptor due to excessive buildup of plaque on the vessel wall. Invasive percutaneous coronary intervention (PCI) procedures such as atherectomy, balloon angioplasty, and stent deployment restore the blood flow in diseased coronary arteries. However, in-stent restenosis, which is the re-narrowing of the vessel as a response to wall injury and endothelial denudation, is one of the major drawbacks of this procedure [[2], [3], [4]]. Following stent deployment, endothelial denudation and exposure of the vessel wall to blood flow results in immediate platelet and fibrinogen adherence to the vessel wall, and the adhesion of leukocytes. In addition to circulating cells adhering to the lumen, vessel wall injury due to the high-pressure distension causes medial smooth muscle cells (SMC) and adventitial cell damage, followed by their proliferation and migration to the lumen surface [[5], [6], [7]]. In an effort to prevent the resulting intimal hyperplasia, drug-eluting stents (DES) were developed roughly 15 years ago. Currently marketed DES deliver antiproliferative drugs, mammalian target for rapamycin (mTOR) inhibitors (sirolimus, everolimus, biolimus A9, or zotarolimus), microtubule inhibitors (paclitaxel), or calcineurin blockers (tacrolimus or pimecrolimus) to the vessel injury site, and reduce in-stent restenosis while avoiding systemic toxicity [8,9]. However, the non-specific antiproliferative effect of eluted drugs affects not only SMCs but also endothelial cells (EC), which results in the need for prolonged antiplatelet therapy following stent deployment [10,11]. Although re-endothelialization between the stent struts of some of the newer DESs, such as everolimus-eluting stents, is comparable with that of bare metal stents, eNOS expression in the repopulated ECs of vessels with DES are significantly lower than those with bare metal stents (BMS) [12,13]. Moreover, treatment failures with first- and second-generation DES is still too common: the COMPARE trial reported that 11.4% of patients required target-vessel revascularization at 5 years for paclitaxel-eluting stents (1st generation DES), and 7.4% revascularization for everolimus-eluting stents (2nd generation DES) [14]. Similarly, the RESOLUTE trial showed total cardiac event accrual of 15% at 5 years, including a 10% target vessel revascularization rate, due mainly to in-stent restenosis but also due to acute thrombosis. Patients with early in-stent restenosis - occurring before one year - had higher incidences of myocardial infarction (MI) and death as compared to other patients [15]. Thus, while DES certainly function better than bare-metal stents – which have a 30% restenosis rate – there are still major limitations to currently available DES for cardiac patients [16,17]. Given the substantial use of these devices in countries like the US, there is an urgent need for a novel stent technology which prevents SMC proliferation more potently than currently available DES, and which differentiates its inhibitory effect between SMCs and ECs, thereby sparing endothelial function.