The plasma membrane(PM)plays an essential role in maintaining cell homeostasis,therefore,timely and effective repair of damage caused by factors such as mechanical rupture,pore-forming toxins,or pore-forming proteins ...The plasma membrane(PM)plays an essential role in maintaining cell homeostasis,therefore,timely and effective repair of damage caused by factors such as mechanical rupture,pore-forming toxins,or pore-forming proteins is crucial for cell survival.PM damage induces membrane rupture and stimulates an immune response.However,damage resulting from regulated cell death processes,including pyroptosis,ferroptosis,and necroptosis,cannot be repaired by simple sealing mechanisms and thus,requires specialized repair machinery.Recent research has identified a PM repair mechanism of regulated cell death-related injury,mediated by the endosomal sorting complexes required for transport(ESCRT)machinery.Here,we review recent progress in elucidating the ESCRT machinery-mediated repair mechanism of PM injury,with particular focus on processes related to regulated cell death.This overview,along with continued research in this field,may provide novel insights into therapeutic targets for diseases associated with dysregulation of regulated cell death pathways.展开更多
文摘MG53(mitsugumin 53)蛋白,是E3泛素连接酶多功能三结构域(tripartite motif,TRIM)蛋白家族成员之一,又被称为TRIM72。MG53是一种细胞膜修复蛋白,广泛表达于心肌和骨骼肌,可在膜损伤部位快速积累,在骨骼肌和心肌细胞膜修复中发挥重要作用。近年来,大量研究发现,MG53可以参与缺血预适应和缺血后适应的心肌保护作用,减轻心肌缺血再灌注损伤;并且在生理或病理状态下,MG53在许多器官中均有表达,促进细胞膜修复。然而MG53过表达则会导致泛素依赖的胰岛素受体表达下降,进而导致代谢综合征和糖尿病性心脏病。本文综述了近年来MG53的生理功能及其相关作用机制研究进展,以期为重组人MG53(recombinant human mitsugumin53,rhMG53)的临床应用提供参考。
文摘The plasma membrane(PM)plays an essential role in maintaining cell homeostasis,therefore,timely and effective repair of damage caused by factors such as mechanical rupture,pore-forming toxins,or pore-forming proteins is crucial for cell survival.PM damage induces membrane rupture and stimulates an immune response.However,damage resulting from regulated cell death processes,including pyroptosis,ferroptosis,and necroptosis,cannot be repaired by simple sealing mechanisms and thus,requires specialized repair machinery.Recent research has identified a PM repair mechanism of regulated cell death-related injury,mediated by the endosomal sorting complexes required for transport(ESCRT)machinery.Here,we review recent progress in elucidating the ESCRT machinery-mediated repair mechanism of PM injury,with particular focus on processes related to regulated cell death.This overview,along with continued research in this field,may provide novel insights into therapeutic targets for diseases associated with dysregulation of regulated cell death pathways.
