自噬
内体
溶酶体
内吞作用
神经退行性变
mTORC1型
程序性细胞死亡
内吞循环
TFEB
粒体自噬
细胞
信号转导
细胞生物学
生物
细胞内
PI3K/AKT/mTOR通路
生物化学
细胞凋亡
酶
医学
疾病
病理
作者
Hemmo Meyer,Bojana Kravić
标识
DOI:10.1146/annurev-biochem-030222-102505
摘要
Lysosomes are the degradative endpoints of material delivered by endocytosis and autophagy and are therefore particularly prone to damage. Membrane permeabilization or full rupture of lysosomal or late endosomal compartments is highly deleterious because it threatens cellular homeostasis and can elicit cell death and inflammatory signaling. Cells have developed a complex response to endo-lysosomal damage that largely consists of three branches. Initially, a number of repair pathways are activated to restore the integrity of the lysosomal membrane. If repair fails or if damage is too extensive, lysosomes are isolated and degraded by a form of selective autophagy termed lysophagy. Meanwhile, an mTORC1-governed signaling cascade drives biogenesis and regeneration of new lysosomal components to reestablish the full lysosomal capacity of the cell. This damage response is vital to counteract the effects of various conditions, including neurodegeneration and infection, and can constitute a critical vulnerability in cancer cells.
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