Highlighted Articles - Atherosclerosis September 2015 Issue
17 September 2015
Volume 242 Issue 1 September 2015
By Elvira Mambetisaeva, Sarah Leigh and Steve Humphries (Editor–in-Chief)
Using clonal populations of valvular endothelial cells (VECs) and valvular interstitial cells (VICs) in a series of elegant experiments, Hjortnaes et al were able to test their hypothesis that aortic VECs undergo osteogenic differentiation via an endothelial-to-mesenchymal transformation process that can be inhibited by VICs. Their data supported this hypothesis and is significant as it highlights the importance of VEC–VIC interactions in valve homeostasis. In their invited Discussion article “Valvular endothelial cells: Guardians or destroyers of aortic valve integrity?”, Rattazzi & Pauletto give a detailed overview of current research into the field of valve homeostasis, welcoming the contribution of Hjortnaes et al and concluding that future studies will need to focus on cellular and molecular targets aimed at preventing and arresting calcific valve disease.
Jung et al used the Korean Heart Study which consists 200,100 Korean adults, to evaluate the performance of the American College of Cardiology/American Heart Association (ACC/AHA) 2013 Pooled Cohort Equations. The study also aimed to develop Korean Risk Prediction Model (KRPM) for atherosclerotic cardiovascular disease (ASCVD) events by following the subjects of the study for more than 10 years. Jung et al found that regardless of whether the ‘White’ or ‘ African-American’ version of equation was used, the unadjusted AHA-ACC-ASCVD risk scores overestimated ASCVD events in Korean men, but AHA-ACC-ASCVD risk score designed for ‘White’ underestimated events in Korean women. In their invited commentary DeFilippis & Blaha point out that this finding in Korean men was not unexpected as other researchers observed that AHA-ACC-ASCVD risk score overestimated risk in different cohorts. DeFilippis & Blaha highly praise a new KHS based score which showed ‘superior calibration and discrimination as compared to the AHA-ACC-ASCVD risk score in its native form.’
The review by Lee & Tontonoz discusses the role of sterol-responsive transcription factors Liver X Receptors (LXRs) in maintaining cholesterol homeostasis. These molecules are activated physiologically by oxidized derivatives of cholesterol, oxisterols, which are synthesised when cells accumulate excess cholesterol. The authors focus on recent findings on atheroprotective gene targets of LXRs and elucidate the molecular mechanisms of beneficial LXR-mediated effects on cholesterol metabolism.
The role of B cells in abdominal aortic aneurysm (AAA) was summarised in a review by Zhang & Wang. Many studies have confirmed that AAA is an immune-related disease where large amounts of B cells have been found. B cells also act as antigen-presenting cells to activate T-cells and they produce cytokines and immunoglobulins, resulting in the activation of macrophages, mast cells and complement pathways. However, the precise mechanisms of B-cells functions in development of AAA have still to be clarified.
Borow et al in their review article describe the beneficial pleiotropic effects of eicosapentaenoic acid (EPA), an omega-3 polyunsaturated fatty acid, on the atherosclerosis processes such as plaque development, plaque rupture and thrombus formation. The authors discuss the biological plausibility of EPA as an anti-atherosclerotic agent.
Papers in this issue include: