Endothelial progenitor cells: Exploring the pleiotropic effects of statins

Abstract

Statins have become a cornerstone of risk modification for ischaemic heart disease patients. A number of studies have shown that they are effective and safe. However studies have observed an early benefit in terms of a reduction in recurrent infarct and or death after a myocardial infarction, prior to any significant change in lipid profile. Therefore, pleiotropic mechanisms, other than lowering lipid profile alone, must account for this effect. One such proposed pleiotropic mechanism is the ability of statins to augment both number and function of endothelial progenitor cells. The ability to augment repair and maintenance of a functioning endothelium may have profound beneficial effect on vascular repair and potentially a positive impact on clinical outcomes in patients with cardiovascular disease. The following literature review will discuss issues surrounding endothelial progenitor cell (EPC) identification, role in vascular repair, factors affecting EPC numbers, the role of statins in current medical practice and their effects on EPC number.

Statins Suppress Ebola Virus Infectivity by Interfering with Glycoprotein Processing

“…The results of this study clearly show that statin inhibits EBOV infection. Our results, combined with statins' known role in suppressing inflammation (74) and preserving endothelial integrity (75), pathways that are impaired in EVD, argue for a potential benefit of using statins as adjunctive therapy in patients with EVD. Ideally, the use of an antiviral that exhibits additional effects in combination with a statin has the potential both to block virus replication and to decrease the deleterious effects of inflammation on the host.…”

The PI3k/Akt Pathway Is Associated With Angiogenesis, Oxidative Stress and Survival of Mesenchymal Stem Cells in Pathophysiologic Condition in Ischemia

“…Statins are able to increase eNOS expression by inhibiting isoprenylation of Rho GTPase. Statins can also rapidly induce the phosphorylation and activation of eNOS via PI3K/Akt pathway (Gazzerro et al 2012, Sandhu et al 2017.…”

“…Statins have antioxidant pleiotropic effect, which can include indirect mechanism increasing NO bioavailability accounting for antioxidant properties. Secondly, statin therapy has also been shown to inhibit activation of NAD(P)H oxidase and ROS release and activation of catalase and thioredoxin ROS scavenging mechanisms (Sandhu et al 2017).…”

Characterization and Functional Assessment of Endothelial Progenitor Cells in Ischemic Stroke Patients

“…For example, it was demonstrated that diabetes mellitus [ 46 ], smoking [ 45 ], hypertension [ 47 ] and atherosclerosis [ 48 ] showed no effect on the quantity of EPCs. However, samples from patients treated with statins showed a correlation between quantity and/or functionality of EPCs with hyperlipidemia, hypertension, diabetes mellitus and atrial fibrillation [ 5 , 49 ]. The present results, which also demonstrated a lack of significant difference in the quantity of EPCs in relation to the presence or absence of screened vascular risk factors, are consistent with the previous findings.…”