Preface: Pathology and Pharmacology of Atherosclerosis

Abstract

Acute cardiovascular syndromes (ACS) such as myocardial infarction, stroke and peripheral artery disease are the leading cause of mortality worldwide. The underlying pathology of ACS is the development of atherosclerosis in the large arteries, which starts already early in life and progresses for decades in a rather silent fashion. Eventually, an advanced atherosclerotic plaque can rupture, or erode, leading to the formation of an occluding thrombus and the subsequent incidence of an acute cardiovascular event. These acute complications are associated with impairment of heart or brain function, and reduce the quality of life for many years. Existing pharmacologic intervention strategies to limit atherosclerosis progression are primarily based on lowering plasma cholesterol levels, for example using statins, which however appear to be insufficient for almost seventy percent of the highrisk patients. New pharmacologic interventions may contribute to the prevention of disease progression, and insights into the mechanisms behind the development of atherosclerosis may identify such novel therapeutic targets. In this theme issue of the European Journal of Pharmacology, entitled “Pathology and Pharmacology of Atherosclerosis”, we aimed to highlight a number of aspects in atherosclerosis development and progression, which may be of interest for novel drug development. To obtain new targets of intervention, experimental models of disease are mandatory, and in this theme issue, Emini Veseli et al. (2017) describes the currently used and novel animal models in atherosclerosis research, from genetically modified mouse models to rabbits and swines. A relatively new approach to induce atherosclerosis in C57BL/6J mice, involving overexpression of PCSK9 (Bjørklund et al, 2014), an enzyme that binds the LDL receptor and directs it for lysosomal degradation, is also addressed