OMIA 002063-9823 : Hyperlipidaemia/atherosclerosis due to ApoE knockout in Sus scrofa

In other species: rabbit

Possibly relevant human trait(s) and/or gene(s) (MIM number): 107741

Mendelian trait/disorder: unknown

Considered a defect: unknown

Species-specific description: This trait results from genetic modification via CRISPR/cas9: the affected animals are genetically-modified organisms (GMO).

Molecular basis: Fang et al. (2018): "clustered regularly interspaced short palindromic repeats (CRISPR)-associated protein 9 system (CRISPR/Cas9) was used to disrupt the ApoE gene in Bama miniature pigs. Biallelic-modified ApoE pigs with in-frame mutations (ApoEm/m ) and frameshift mutations (ApoE-/- ) were simultaneously produced. ApoE-/- pigs exhibited moderately increased plasma cholesterol levels when fed with a regular chow diet, but displayed severe hypercholesterolemia and spontaneously developed human-like atherosclerotic lesions in the aorta and coronary arteries after feeding on a high-fat and high-cholesterol (HFHC) diet for 6 months. Thus, these ApoE-/- pigs could be valuable large animal models for providing further insight into translational studies of atherosclerosis."

Associated gene:

Symbol Description Species Chr Location OMIA gene details page Other Links
APOE apolipoprotein E Sus scrofa 6 NC_010448.4 (51373113..51375333) APOE Homologene, Ensembl, NCBI gene


2018 Fang, B., Ren, X., Wang, Y., Li, Z., Zhao, L., Zhang, M., Li, C., Zhang, Z., Chen, L., Li, X., Liu, J., Xiong, Q., Zhang, L., Jin, Y., Liu, X., Li, L., Wei, H., Yang, H., Li, R., Dai, Y. :
Apolipoprotein E deficiency accelerates atherosclerosis development in miniature pigs. Dis Model Mech 11:, 2018. Pubmed reference: 30305304. DOI: 10.1242/dmm.036632.

Edit History

  • Created by Frank Nicholas on 30 May 2019
  • Changed by Frank Nicholas on 30 May 2019