Department of Medicine II, Saarland University Hospital, Homburg, Germany.
Alcohol Clin Exp Res. 2011 May;35(5):800-3. doi: 10.1111/j.1530-0277.2010.01401.x. Epub 2011 Feb 1.
Genetic risk factors play critical roles in liver injury and fibrosis, since both initiation and progression of chronic liver diseases differ between individuals challenged by identical environmental factors. Recently genomewide association studies have identified specific novel risk genes for (non-alcoholic) fatty liver disease (adiponutrin), viral hepatitis (interleukin 28B), and chronic cholestatic diseases (interleukin 12). Here, we summarize these studies and provide an inventory of the susceptibility genes. In the future, risk assessment of complex liver diseases might be based on polygenic risk scores or even gene networks. Complimentary to study in humans, experimental crosses of inbred mouse strains contribute to the genetic dissection of gene-gene interaction and gene-environment interactions. The results of these genomewide studies in mice and men might open new avenues for the prevention and treatment of chronic liver injury and the regression of liver fibrosis.
遗传风险因素在肝损伤和纤维化中起着关键作用，因为在相同环境因素的挑战下，慢性肝病的起始和进展在个体之间存在差异。最近的全基因组关联研究已经确定了（非酒精性）脂肪肝疾病（脂联素）、病毒性肝炎（白细胞介素 28B）和慢性胆汁淤积性疾病（白细胞介素 12）的特定新的风险基因。在这里，我们总结了这些研究，并提供了易感性基因的清单。将来，复杂肝脏疾病的风险评估可能基于多基因风险评分，甚至是基因网络。作为人类研究的补充，近交系小鼠的杂交实验有助于基因-基因相互作用和基因-环境相互作用的遗传剖析。这些在小鼠和人类中的全基因组研究的结果可能为慢性肝损伤的预防和治疗以及肝纤维化的消退开辟新途径。
