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CRISPR/Cas9-mediated knockout of APOC3 stabilizes plasma lipids and inhibits atherosclerosis in rabbits.

Yiwen ZhaYaoyao LuTing ZhangKunning YanWenwen ZhuangJingyan LiangYong ChengYingge Wang
Published in: Lipids in health and disease (2021)
APOC3 deficiency can delay the formation of atherosclerosis-induced HFD in rabbits, indicating this is a novel therapeutic target to treat atherosclerosis.
Keyphrases
  • crispr cas
  • cardiovascular disease
  • genome editing
  • high glucose
  • high fat diet
  • diabetic rats
  • type diabetes
  • fatty acid
  • skeletal muscle
  • insulin resistance
  • endothelial cells
  • replacement therapy
  • wild type