基础医学与临床 ›› 2016, Vol. 36 ›› Issue (1): 116-120.
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仲昭宇1,田野2,杨力明1,李弘3
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摘要： TFEB作为一种新型转录因子，可由mTOR、细胞应激等自噬调节因子激活，介导自噬、溶酶体相关基因以及过氧化物酶体增殖物激活受体α（PPAR α)、过氧化物酶体增殖活化受体γ共激活因子-1α(PGC-1α)的表达，促进脂质外排、抑制炎性因子释放。TFEB调节脂质代谢可作为一种新机制，起到抑制动脉粥样硬化进展、稳定斑块的作用。
关键词: 转录因子EB, 动脉粥样硬化, 自噬, PPAR α, PGC-1α
Abstract: TFEB could induced by autophagic regulatory factors, such as mTOR and cellular stresses. TFEB could media the translation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha(PPAR α), peroxisome proliferator-activated receptor γ coactivator 1 α(PGC-1α) and autophagy, lysosomal synthesis related genes, then regulat lipid metabolism and the release inflammatory cytokine. AS a novel Mechanism, TFEB could regulate Lipid metabolism in order to restrain the progression of atherosclerosis and promote to plaque stabilization.
Key words: TFEB , atherosclerosis, autophagy, PPAR α, PGC-1α
仲昭宇 田野 杨力明 李弘. TFEB调控脂质代谢稳定动脉粥样硬化斑块的新机制[J]. 基础医学与临床, 2016, 36(1): 116-120.
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