粒体自噬
自噬
程序性细胞死亡
细胞器
细胞生物学
炎症
细胞
生物
免疫学
细胞凋亡
生物化学
作者
Yu Duan,Ren-qi Yao,Hua Ling,Liyu Zheng,Qi Fan,Qiong Li,Lu Wang,Qi-yuan Zhou,Le-Min Wu,Xingui Dai,Yong-ming Yao
标识
DOI:10.1016/j.jare.2024.05.012
摘要
Dysregulated alterations in organelle structure and function have a significant connection with cell death, as well as the occurrence and development of inflammatory diseases. Maintaining cell viability and inhibiting the release of inflammatory cytokines are essential measures to treat inflammatory diseases. Recently, many studies have showed that autophagy selectively targets dysfunctional organelles, thereby sustaining the functional stability of organelles, alleviating the release of multiple cytokines, and maintaining organismal homeostasis. Organellophagy dysfunction is critically engaged in different kinds of cell death and inflammatory diseases. We summarized the current knowledge of organellophagy (e.g., mitophagy, reticulophagy, golgiphagy, lysophagy, pexophagy, nucleophagy, and ribophagy) and the underlying mechanisms by which organellophagy regulates cell death. We outlined the potential role of organellophagy in the modulation of cell fate during the inflammatory response to develop an intervention strategy for the organelle quality control in inflammatory diseases.
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