Atherosclerosis Mechanism Research: Investigate the impact of functional loss of macrophage scavenger receptor A (SR-A, encoded by the Msr1 gene) on foam cell formation, lipid accumulation, and the initiation and progression of atherosclerotic plaques. Evaluate the role of Msr1 point mutations in atherosclerosis susceptibility, plaque stability, and inflammatory responses. Macrophage Biology and Function Research: Explore the effects of specific Msr1 point mutations on macrophage-mediated apoptotic cell clearance, endogenous ligand recognition, and inflammatory signaling. Study the regulation of macrophage phenotypic polarization, migration, and phagocytic function by Msr1 mutations. Metabolic Syndrome-Related Research: Investigate the role of Msr1 dysfunction in metabolic disorders such as obesity, insulin resistance, and non-alcoholic fatty liver disease. Assess the impact of Msr1 point mutations on systemic metabolic homeostasis and metabolic inflammation. Infection and Immunity Research: Study the role of Msr1 in recognizing pathogen-associated molecular patterns, mediating bacterial clearance, and regulating anti-infective immune responses. Evaluate the impact of Msr1 point mutations on susceptibility to specific bacterial infections (e.g., Streptococcus pneumoniae, Mycobacterium tuberculosis).

1. Research on type 2 diabetes and metabolic diseases: Simulating the physiological and pathological functions of human glucagon receptor (GCGR) to study its regulatory mechanisms in glucose homeostasis, glycogenolysis, fatty acid metabolism, and energy balance, and constructing metabolic disease models closer to human diseases. 2. Evaluation of GCGR-targeted drugs: Evaluating the pharmacodynamics, pharmacokinetics, and safety of antibodies, peptides, and small molecule antagonists/agonists targeting human GCGR in vivo, providing an ideal preclinical model for the development of new hypoglycemic drugs or drugs for treating non-alcoholic fatty liver disease (NASH) and other diseases. 3. Research on the glucagon signaling pathway: Under the background of complete humanized receptors, exploring the specific role of the glucagon-GCGR signaling axis in the liver, pancreas, kidney, and central nervous system, as well as its interactions with other hormone pathways (such as insulin).

1. Research on Hyperuricemia and Gout: Studying the molecular mechanisms of pathogenic processes such as elevated blood uric acid levels, urate crystal deposition, and gouty arthritis caused by the deficiency of urate oxidase (UOX) is a classic model for simulating human hyperuricemia and gout. Evaluate the efficacy of uric acid-lowering drugs (such as allopurinol, febuxostat) and anti-inflammatory drugs in the acute attack and chronic management of gout. 2. Metabolic Syndrome and Kidney Damage: Explore the impact of chronic hyperuricemia on kidney function, study the association mechanisms of uric acid-related kidney damage (such as uric acid nephropathy, kidney stones) and metabolic syndrome (hypertension, insulin resistance). 3. Cardiovascular Disease Research: Assess the role of hyperuricemia in the occurrence and development of cardiovascular diseases such as atherosclerosis, hypertension, and heart failure.

. Atherosclerosis and Cardiovascular Disease Research: Investigate the mechanism of plasma low-density lipoprotein (LDL) clearance disorder, severe hypercholesterolemia, and spontaneous atherosclerotic plaque formation caused by low-density lipoprotein receptor (LDLR) deficiency. Under the induction of a high-fat diet (such as the Western diet), accelerate the progression of atherosclerotic lesions, and evaluate the efficacy of lipid-lowering drugs (such as statins, PCSK9 inhibitors), anti-inflammatory drugs, or novel intervention methods. 2. Lipid Metabolism and Liver Physiopathology: Explore the core role of LDLR in liver lipid uptake, metabolism, and cholesterol homeostasis, and study its impact on the development of non-alcoholic fatty liver disease (NAFLD) and liver fibrosis. 3. Metabolic Syndrome Research: Assess the impact of LDLR deficiency on systemic lipid metabolism disorder, insulin resistance, and obesity-related metabolic abnormalities.

1. Research on atherosclerosis and cardiovascular diseases: Studying the dyslipidemia caused by ApoE deficiency (such as hypercholesterolemia), spontaneous formation and progression of atherosclerotic plaques, and their pathogenic mechanisms. Evaluating the preventive and therapeutic effects of lipid-lowering drugs (such as statins, PCSK9 inhibitors), anti-inflammatory therapies, or novel intervention methods on atherosclerotic lesions. 2. Lipid metabolism and liver physiology: Exploring the core role of ApoE in lipoprotein assembly, transport, and clearance, and studying its impact on liver lipid metabolism and the development of non-alcoholic fatty liver disease (NAFLD). 3. Research on neurodegenerative diseases (such as Alzheimer's disease): Using ApoE KO mice combined with high-fat diet and other interventions to study the associations between dyslipidemia, intracerebral cholesterol metabolism disorders, cognitive dysfunction, and pathological processes such as β-amyloid deposition.

1. Research on phosphorus transport and metabolic homeostasis: Investigate the effects of X-phosphatase transport protein 1 (XPR1) deficiency on cellular and systemic inorganic phosphorus (Pi) transport and homeostasis maintenance, study its role in skeletal development, mineralization, and renal phosphorus reabsorption, and establish related phosphorus metabolism disorder models. 2. Viral host interactions and endogenous retrovirus research: Evaluate the function of XPR1 as a key receptor for various exogenous retroviruses (such as XPR1-dependent strains of mouse leukemia virus MLV) and endogenous retroviruses (ERV), and study the effects of XPR1 deficiency on viral invasion, replication, and latent infection. 3. Tumor biology and tumor virology: Study the role of XPR1-mediated phosphorus signaling pathway in tumor cell proliferation and metabolic reprogramming, and assess its potential as a tumor therapeutic target. Explore the potential role of XPR1 in the pathogenic mechanism of tumor-associated viruses.

1. Research on oxidative stress and antioxidant defense mechanisms: Investigate the effect of Bach1 transcription factor deficiency on the expression of genes regulated by classical antioxidant response elements (ARE) such as HO-1 and NQO1, clarifying its core regulatory role in cellular antioxidant stress response. Explore the role of Bach1 in oxidative stress-related pathological processes such as ischemia-reperfusion injury and neurodegenerative diseases. 2. Iron metabolism and iron death research: Assess the regulation of Bach1 deficiency on the expression of iron metabolism-related genes (such as ferritin, transferrin receptor) and its impact on intracellular iron homeostasis and iron death sensitivity. Explore the therapeutic potential of targeting the Bach1-HO-1 pathway in regulating iron death and related diseases (such as tumors, neurodegenerative diseases). 3. Tumor biology and immune microenvironment: Study the role of Bach1 in tumor cell proliferation, invasion, metastasis, and metabolic reprogramming. Evaluate the impact of Bach1 deficiency on immune cell function in the tumor microenvironment (such as macrophage polarization, T cell activity) and anti-tumor immune response.

1. Atherosclerosis and Cardiovascular Disease Research: Investigate the mechanism of action of Treml1 in the formation, progression, and destabilization of atherosclerotic plaques. Assess the impact of Treml1 deficiency on macrophage inflammatory response, lipid metabolism, and vascular endothelial function. 2. Immune and Inflammatory Regulation: Explore the regulatory functions of Treml1 in innate immunity (such as macrophages, dendritic cells) and adaptive immunity (such as T cells). Establish models of inflammatory diseases (such as sepsis, rheumatoid arthritis) to study the role of Treml1 in inflammatory responses. 3. Metabolic Syndrome Research: Evaluate the role of Treml1 in metabolic disorders such as obesity, insulin resistance, and non-alcoholic fatty liver disease (NAFLD).

Metabolism and Obesity Research: Investigate the effects of Dusp13b (a dual-specificity phosphatase) deficiency on glycolipid metabolism, energy balance, and the development of obesity. Explore the role of Dusp13b in insulin signaling pathways, glucose homeostasis, and the regulation of adipose tissue function. Cardiovascular Disease Research: Assess the role of Dusp13b in cardiovascular stress, myocardial hypertrophy, and heart failure. Study the impact of Dusp13b deficiency on cardiovascular system function and related signaling pathways (e.g., MAPK pathway). Cellular Stress and Apoptosis Research: Investigate the regulatory function of Dusp13b in cellular stress responses, oxidative stress, and apoptosis. Evaluate the potential role of Dusp13b in tumor cell proliferation, migration, and drug resistance.

Inflammation and Immunology Research: Investigate the role of 12/15-lipoxygenase (Alox15) in acute and chronic inflammatory responses. Explore the mechanisms of Alox15 and its metabolites in inflammatory diseases (e.g., arthritis, asthma, inflammatory bowel disease). Metabolic Disease Research: Assess the role of Alox15 and related signaling pathways in metabolic diseases (e.g., atherosclerosis, diabetes, obesity). Investigate the regulatory functions of Alox15 in lipid metabolism, insulin resistance, and adipose tissue inflammation. Neurobiology and Cancer Research: Explore the potential role of Alox15 in neuroinflammation and neurodegenerative diseases (e.g., Alzheimer's disease). Study the impact of Alox15 in the development of specific tumor microenvironments (e.g., inflammation-related cancers).

Metabolism Research: Investigate the impact of Acylglycerol Kinase (AGK) E3 isoform knockout on lipid metabolism and energy homeostasis. Explore models of metabolic syndrome associated with AGK dysfunction. Cardiovascular Research: Study the role of AGK in myocardial lipid metabolism, cardiac function maintenance, and the development of heart failure. Establish research models for dilated or hypertrophic cardiomyopathy. Endocrinology Research: Investigate the potential role of AGK in hormone synthesis and signaling.

Hypertension Research?