蛋白质泛素化修饰及其在脓毒症中的研究进展

Protein Ubiquitination Modification and Its Research Progress in Sepsis

蛋白质在机体生命活动中扮演关键角色,其降解途径中,泛素-蛋白酶体途径(UPS)通过泛素化修饰调控蛋白降解,同时通过共价修饰底物蛋白参与细胞生理活动。去泛素化酶(DUBs)对蛋白质泛素化具有平衡作用,通过移除泛素化修饰来维持泛素化修饰的动态平衡,它们在脓毒症中发挥着关键作用,通过调控炎症因子的表达,影响机体的炎症反应。脓毒症是导致患者重症监护的主要疾病,涉及复杂炎症反应。蛋白质泛素化修饰参与脓毒症信号转导,影响核因子-κB(NF-κB)信号通路和NOD样受体蛋白3炎症小体(NLRP3)活化。这些调控机制影响细胞内炎症因子的释放,进而影响机体炎症反应的强度和时机。本文探讨了近年来与脓毒症相关关键蛋白的泛素化及去泛素化机制,以期为脓毒症的治疗提供新的靶点和策略。

Proteins play crucial roles in the vital activities of organisms.In their degradation pathway,the ubiquitin-proteasome system(UPS)regulates protein degradation through ubiquitination modification,while participates in cellular physiological activities by covalently modifying substrate proteins.Deubiquitinating enzymes(DUBs)balance protein ubiquitination by removing ubiquitin modifications,playing a key role in sepsis by regulating the expression of inflammatory factors.Sepsis is a major disease leading to intensive care for patients,involving complex inflammatory responses.Protein ubiquitination modification is involved in sepsis signal transduction,affecting the nuclear factorκB(NF-κB)signaling pathway and the activation of NOD-like receptor protein 3(NLRP3)inflammasomes.These regulatory mechanisms influence the release of intracellular inflammatory factors,thereby affecting the intensity and timing of the body's inflammatory response.This article discusses recent research on the ubiquitination and deubiquitination mechanisms of key proteins related to sepsis,aiming to provide new targets and strategies for sepsis treatment.