Coagulation and Thrombosis Research: Investigate the role of human coagulation factor X (F10) in the intrinsic and extrinsic coagulation pathways, thrombin generation, and pathological thrombosis. Evaluate the pathophysiological mechanisms of coagulation factor X in thrombotic diseases such as atherosclerosis and deep vein thrombosis. Anticoagulant Drug Development and Evaluation: Evaluate the pharmacodynamics, pharmacokinetics, and bleeding risks of direct oral anticoagulants (e.g., rivaroxaban, apixaban) and other novel inhibitors targeting human coagulation factor X in vivo. Study the therapeutic effects of coagulation factor X inhibitors in different thrombosis models. Hemophilia Treatment Research: Simulate reduced activity or dysfunction of coagulation factor X to study the bleeding phenotypes of hemophilia (particularly hemophilia A/B) and the efficacy of replacement therapies. Evaluate the preclinical efficacy of novel gene therapies, long-acting factor products, and non-factor replacement therapies based on coagulation factor X. Hemostasis and Surgical Research: Investigate the changes and regulation of human coagulation factor X in acquired coagulation disorders such as trauma, surgery, and liver disease. Assess the balancing role of coagulation factor X in physiological hemostasis and pathological hyperfibrinolysis.

Cohesinopathy Mechanism Research: Investigate the role of Smc1a gene deficiency in the pathogenesis of Cornelia de Lange syndrome and other cohesinopathy-related disorders. Evaluate the impact of cohesin Smc1a subunit deficiency on chromosome cohesion, sister chromatid separation, and genomic stability. Embryonic Development and Organogenesis Research: Explore the critical functions of Smc1a during early embryonic development and organ formation processes. Study the developmental defects, growth retardation, and multi-system developmental abnormalities resulting from Smc1a deficiency. Neurodevelopment and Function Research: Investigate the effects of Smc1a deficiency on nervous system development, neuronal migration, synapse formation, and cognitive function. Assess the application of Smc1a KO mice in modeling neurodevelopmental disorders (such as autism spectrum disorders, intellectual disability). Tumorigenesis and DNA Damage Response: Study the role of Smc1a in maintaining genomic stability, DNA damage repair, and cell cycle regulation. Evaluate the impact of Smc1a deficiency on tumor susceptibility, cell proliferation, and apoptosis.

Progeria Mechanism and Therapeutic Research: Investigate the molecular and cellular mechanisms by which Lamin A gene mutations cause Hutchinson-Gilford progeria syndrome. Evaluate the in vivo efficacy and safety of potential therapies for progeria (e.g., farnesyltransferase inhibitors, gene therapy) in this model. Cardiovascular and Atherosclerosis Research: Study accelerated vascular aging, arterial stiffness, and atherosclerosis progression in the progeria model. Test intervention strategies aimed at protecting vascular function and delaying vascular aging. Metabolism and Systemic Aging Research: Explore systemic metabolic disorders, lipodystrophy, insulin resistance, and other phenotypes in the progeria model. Evaluate the therapeutic effects of drugs aimed at improving metabolic function and delaying multi-system aging. Aging-Related Drug Screening: Serve as an accelerated aging model for screening and evaluating potential anti-aging drugs and compounds that protect cardiovascular and metabolic function.

1. Research on the specific functions of nuclear lamins A/C: By combining tissue-specific Cre-loxP tools in mice, the LMNA gene is conditionally knocked out in specific cell types (such as cardiomyocytes, skeletal muscle cells, adipocytes, fibroblasts, etc.) to study the specific functions of nuclear lamins A/C in tissue development, homeostasis, and diseases. 2. Exploration of the mechanisms of laminopathy and premature aging syndrome: Constructing specific LMNA deficiency models in myocardium, skeletal muscle, or adipose tissue, simulating and studying the pathogenesis of different types of laminopathies (such as Emery-Dreifuss muscular dystrophy, dilated cardiomyopathy, familial partial lipodystrophy) and Hutchinson-Gilford progeria syndrome. 3. Research on nuclear structure and function: Studying the effects of LMNA deficiency or mutation on nuclear structure (nuclear membrane integrity, chromatin organization), gene expression, DNA damage repair, and cellular aging.

1. Hemophilia B Disease Model and Pathological Mechanism Research: Simulating human factor IX (FIX) deficiency, studying the pathophysiological processes of bleeding phenotype, joint lesions, and long-term complications in hemophilia B. Evaluating the in vivo pharmacodynamics, pharmacokinetics, and hemostatic effects of FIX replacement therapies (such as recombinant FIX, long-acting FIX products). 2. Gene Therapy and New Therapy Assessment: Evaluating the long-term expression levels, safety, and therapeutic window of FIX gene therapy based on AAV, non-viral vectors, and other carriers. Testing emerging therapies, such as non-factor therapies (such as antibodies against tissue factor pathway inhibitors, siRNA therapy) and gene editing (such as CRISPR/Cas9-mediated gene correction) for their efficacy and safety in the hemophilia B model. 3. Hemostasis and Thrombosis/Coagulation Balance Research: Under the background of introducing human F9 gene, studying the endogenous pathway of the coagulation cascade, as well as the balance strategy of procoagulant/anticoagulant treatment.

1. Hemophilia A Disease Model and Pathological Mechanism Research: Simulating human factor VIII (FVIII) deficiency, studying the pathological physiological processes of hemophilia A, including bleeding tendency, joint lesions, and inflammatory reactions. Evaluating the in vivo pharmacodynamics and pharmacokinetics of FVIII replacement therapies (such as recombinant FVIII, long-acting FVIII products). 2. Gene Therapy and New Therapy Assessment: Evaluating the long-term expression levels, safety, and efficacy of FVIII gene therapy based on vectors such as AAV, lentivirus, etc. Testing emerging therapies, such as non-factor replacement therapies (such as bispecific antibodies, siRNA therapy) and gene editing therapies, for their effects in the hemophilia A model. 3. Hemostasis and Thrombosis Research: Under the background of introducing the human F8 gene, studying the regulatory mechanisms of the coagulation cascade reaction, as well as the balance of anticoagulant/procoagulant treatment.

Amyotrophic Lateral Sclerosis (ALS) Research: Investigate the role of human SOD1 gene mutations (e.g., G93A, G37R) in ALS pathogenesis, modeling the pathological features of familial ALS. Evaluate the efficacy of gene therapies, antisense oligonucleotide therapies, and small molecule drugs targeting mutant human SOD1 protein. Oxidative Stress and Neuroprotection: Study the core function of SOD1 in scavenging superoxide radicals and maintaining redox balance. Explore the association between SOD1 dysfunction, oxidative stress damage, and neurodegenerative diseases (e.g., Alzheimer's disease, Parkinson's disease). Drug Screening and Preclinical Validation: Provide a highly clinically relevant humanized animal model for evaluating the pharmacodynamics and safety of therapeutic strategies targeting the SOD1 pathway or alleviating SOD1-related toxicity.

1、Mechanism studies of aging-related diseases；
2、Development of anti-aging products；