动物模型 z-bo 2022-02-03 442

　　[Modeling mechanism] Use genetic engineering and other experimental techniques to intentionally modify the animal genome. The modified genes are stably inherited by offspring animals, and various mouse models have been established. One type of model is mainly aimed at animal models of cardiomyopathy phenotypes. For example, an animal model that overexpresses RhoA. hoA is a small G protein that regulates the actin backbone. Its overexpression causes sinus nodular dilated cardiomyopathy. And there are atrioventricular node dysfunction and atrial fibrillation. The other type of model is mainly used for electrical remodeling of the myocardium and has nothing to do with signs of cardiomyopathy. For example, in an animal model that overexpresses Kir2.1, Kir2.1 encodes the α subunit of the inwardly rectified potassium current IK1, and its overexpression has an important impact on IK1, which will affect the resting membrane potential and the reproduction of cardiomyocytes. . It changes the polarization stage 3, thus greatly shortening its effect.

　　The underlying time course can cause spontaneous atrial fibrillation. Knockout Linkin 40 mice (CD40-/-, CD40-/ +) have normal atrial development, but may have slower conduction velocity, longer sinus node recovery time, and induce atrial fibrillation. Will be higher. The other type is mainly used to reshape the atrial structure without ventricular dysfunction. For example, in mice overexpressing transforming growth factor β1 (transforming growth factor β1 and TGFβ1), atrial fibrosis is obvious, especially the conduction velocity of the right atrium is significantly reduced, leading to atrial fibrillation. It is easy to induce.

　　[Model Evaluation and Application] This type of model is mainly aimed at mice and can be used to study the molecular mechanism of atrial fibrillation.