Lipoprotein(a) (LP(a)) is considered one of the risk factors for atherosclerosis, coronary heart disease, stroke, and other cardiovascular diseases (CVD) ^[1]. It is similar in size and lipid content to low-density lipoprotein (LDL) and contains the lipoprotein ApoB-100, but also includes a variable-length lipoprotein(a) (Apo(a)), which is covalently bound to ApoB-100 via a single disulfide bond. LP(a) plays an important role in systemic lipid transport, guiding inflammatory cells into the vascular wall and causing smooth muscle cell proliferation. In addition, it is also involved in wound healing and tissue repair, interacting with components of the vascular wall and extracellular matrix ^[2]. LP(a) can also cause arterial narrowing by attaching to the arterial wall, accelerating the formation of blood clots, and leading to a series of pathological changes ^[3].

The plasma concentration of LP(a) is closely related to genetic factors and is mainly regulated by the LPA gene. Therefore, the LPA gene is an important potential target for treating cardiovascular disease. The LPA gene is expressed in humans and non-human primates but not mice. By crossing mice conditional expression of human LPA (LSL-hLPA) with liver-specific Cre expression mice (Alb-Cre) that specifically overexpress the human LPA gene in the liver can be obtained.

ApoB is a protein that plays a central role in lipid metabolism and cardiovascular disease (CVD) and is responsible for transporting cholesterol and other fat molecules to all tissues throughout the body ^[4]. The accumulation of cholesterol and other lipids can promote the formation of arterial plaques, leading to arterial narrowing and reduced blood flow, increasing the risk of cardiovascular events such as myocardial infarction and stroke ^[5]. Therefore, high levels of ApoB are a major risk factor for plaque in cardiovascular diseases such as atherosclerosis. ApoB100 is the most abundant subtype of ApoB in humans and the most important subtype of ApoB in cardiovascular disease (CVD) ^[6]. Mice overexpressing the human APOB gene have significantly elevated LDL cholesterol in serum.

The B6-RCL-hLPA/Alb-cre/TG(APOB) mice express human LP(a) and ApoB, two risk factors for cardiovascular disease. It can be used in the study of hyperlipidemia, stroke, coronary heart disease, familial hypercholesterolemia (FH), and other atherosclerotic cardiovascular diseases (ASCVD). Internal data (not shown) indicates that, compared to the Cyagen strain B6-LPA(CKI)/Alb-Cre&Tg(APOB) mice (Catalog No. C001494), this model exhibits a more stable expression of human LPA protein at different ages. Please choose the model based on the experimental need for continuous stability of human LPA protein expression.