作者
Wenbo Qu,Xin Zhou,Xinjian Jiang,Xianwei Xie,Kai-Jian Xu,Xia Gu,Ruisi Na,Minghui Piao,Xiangwen Xi,Na Sun,Xueyu Wang,Xiang Peng,Junyan Xu,Jiangtian Tian,Jian Zhang,Junli Guo,Maomao Zhang,Yao Zhang,Zhenwei Pan,Kun Wang,Bo Yu,Bin Sun,Shuijie Li,Jinwei Tian
摘要
Current therapies cannot completely reverse advanced atherosclerosis. High levels of amino acids, induced by Western diet, stimulate mTORC1 (mammalian target of rapamycin complex 1)-autophagy defects in macrophages, accelerating atherosclerotic plaque progression. In addition, autophagy-lysosomal dysfunction contributes to plaque necrotic core enlargement and lipid accumulation. Therefore, it is essential to investigate the novel mechanism and molecules to reverse amino acid-mTORC1-autophagy signaling dysfunction in macrophages of patients with advanced atherosclerosis.