PRJNA542758
Establishment and mechanism research of spontaneous serum lipid model based on wild mouse chromosome 1 substitution strains
Hyperlipidemia, as a common chronic disease, seriously affects human health. Building an animal model of dyslipidemia is an important foundation for basic research and drug development. Previous animal models were often established using high-fat diet-induced methods. These models have some defects: poor stability and mechanisms of model formation and human pathogenesis (multi-gene, multi-environmental factors) have significant differences.Through 10 years effort, our research team constructed 25 wild-type replacement chromosome mice. Preliminary phenotypic identification indicated that some strains had abnormal lipid metabolism at 20 weeks of age under non-inducing conditions; whole-genome sequencing data showed that these lines were rich in genetic diversity; some strains of liver gene expression profiles showed relevant pathway genes of lipid metabolism have significant differences in expression levels. This study will select some strains with abnormal blood lipid metabolism, and establish multiple disease models for various lipid indicators (TC, TG, HDL-C, LDL-C). Further improve the phenotypic identification data and liver expression profile data of all models at different ages; use the clinical drug to verify the validity of the model. This study will construct a stable, inherited, practical and efficient disease model supported by multiple polygenic interactions with databases (genomic sequences and expression profiling data).