Content area
Full Text
Received Mar 20, 2017; Accepted Jun 12, 2017
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
1. Introduction
Intracerebral hemorrhage (ICH) is a crucial classification of stroke and has a high rate of mortality and morbidity [1, 2]. The pathogenesis of ICH is complex and influenced by environmental factors and genetic factors. However, its pathogenesis is not yet clear. Hypertension is the most common contributing factor to primary intracerebral hemorrhage. Factors including smoking, drinking, diabetes, and male gender increase the risk further [3–5]. In addition, many studies have shown an inverse association between the level of serum cholesterol and ICH [6]. More importantly, the role of genetics in the pathogenesis of ICH has received wide attention [7, 8]. Epidemiological studies have demonstrated that a history of a first-degree relative with ICH is an independent risk factor for lobar and nonlobar ICH [4]. It has also been reported that a family history of any stroke was a significant risk factor for patients with ICH who were <70 years compared with those who were >70 years [9]. Taken together, the observed differences based on family history indicate that genetic factors play an important role in the incidence of ICH.
CD36 is a type B scavenger receptor, now officially designated as SR-B2, and CD36 gene located in the 7q11.2 chromosome with 17 exons and 16 introns and is expressed on the surface of various cells: platelets, microvascular endothelial cells, monocytes/macrophages, dendritic cells, adipocytes, striated muscle cells, and hematopoietic cells [10, 11]. As a result of its expression in multiple cell types, it can be involved in a variety of biological processes, including transport of oxidized LDL (oxLDL) and fatty acids by macrophages and monocytes,...