Analysis of SOCS3 gene genotype in patients with acute cerebral infarction and its relationship with disease progression

Ischemic stroke, also known as cerebral infarction, refers to the clinical syndrome in which cerebral blood supply disturbance caused by various reasons leads to corresponding neurological deficits [1]. It generally occurs in people over the age of 50 and has a high disability rate worldwide [2]. Its pathogenesis is mainly related to atherosclerosis, vascular lesions, thrombosis, inflammatory factors, and abnormal lipid metabolism. [3]. The mechanism of inflammation is one of the important mechanisms [4]. In early cerebral infarction ischemia, the release of inflammatory mediators prompts circulating leukocytes to scroll and adhesion to damaged vascular endothelium, thus aggressing the inflammation situation [5]. Simple risk factors, which account for 90 % of the risks of cerebral infarction, are hypertension, smoking, excessive waist-to-hip ratio, improper diet, lack of physical exercise, diabetes, excessive drinking, and hyperlipidemia [6]. Beyond this, the heritable variation plays a crucial role in acute cerebral infarction (ACI). ACI is related to many genes, and exploring the genotype distribution of ACI has an important guiding role in the clinical prevention and treatment of this disease.

SOCS family is a group of proteins induced by cytokines, which has been discovered recently [7]. The human SOCS3 gene is located at 17q25.3 and its length is about 850 bp. SOCS3 is related to many diseases and may be used as a molecular marker for the diagnosis and prognosis of diseases, as well as a target gene for specific diseases. SOCS3 functions as a tumor suppressor in hepatocellular carcinoma, a cytokine on macrophage polarization in Leishmania major infection, and a dominator in the pathological angiogenesis in vascular endothelial cells [8], [9], [10]. SOCS3 is a target of miR-3473b, which regulates stroke progression by improving post-stroke neuroinflammation damage [11]. In atherosclerosis, SOCS3 has been proven to be related to platelet activity, which is the mediator of thrombosis [12]. The frequency of the rs8064821 polymorphism A allele of SOCS3 in obese subjects with metabolic syndrome is higher than in obese children with the non-metabolic syndrome, providing that SOCS3 may be associated with fat metabolism [13]. The same polymorphism is also researched in hypertension, and SOCS3 rs8064821 CA genotype is related to the increased possibility of hypertension [14]. In addition to this, inflammation and abnormal lipids metabolism are essential risk factors for ischemic stroke. Thus, we focused on whether SOCS3 rs8064821 polymorphism is also correlated to ischemic stroke in the present study.

In view of the previous research on SOCS3, this study selected 310 patients with ACI to explore the relationship between SOCS3 gene polymorphism and the progression of ACI.

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