The MYBPC3 gene encodes the cardiac isoform of myosin-binding protein C. MYBPC3 is a critical regulator of cardiac contraction, and mutations in this gene are a common cause of hypertrophic cardiomyopathy (HCM). HCM is the most prevalent inherited cardiomyopathy worldwide, following an autosomal dominant inheritance pattern. This condition is marked by unexplained left ventricular hypertrophy, a non-dilated left ventricle with preserved or increased ejection fraction, and myocardial disarray along with interstitial fibrosis. Left ventricular diastolic dysfunction is also common. HCM is a leading cause of sudden cardiac death, particularly in adolescents and young adults ^[1-2]. Research indicates that Mybpc3 homozygous knockout mice exhibit pronounced cardiac hypertrophy and diastolic dysfunction ^[3]. These mice serve as a platform for studying the mechanisms and developing therapeutic approaches for familial hypertrophic cardiomyopathy (FHC). The Mybpc3-KO mouse is a gene knockout model created using gene-editing techniques to knock out the coding sequence of the Mybpc3 gene (the homolog of the human MYBPC3 gene) in mice. The model exhibited increased left ventricular mass and prolonged isovolumic relaxation time (IVRT), with a trend toward enlarged cardiomyocyte cross-sectional area and increased cardiac fibrosis. Meanwhile, left ventricular ejection fraction (LVEF) and fractional shortening (LVFS) showed a decreasing trend compared to controls. This model is used to research the pathogenic mechanisms of hypertrophic cardiomyopathy (HCM) and develop related therapeutic strategies.

Slc9a6 is located on chromosome X of mice. Nuclease Technology was used to design sgRNA; Slc9a6 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.

Aipl1 is located on chromosome 11 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Aipl1 conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.

Mybpc3 is located on chromosome 2 of mice. Nuclease Technology will be used to design sgRNA; Mybpc3 knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.

Mybpc3 is located on chromosome 2 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Mybpc3 conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.