Autophagy in inflammatory diseases.
Autophagy in inflammatory diseases.
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DOI：
10.1155/2011/732798
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发表时间：
2011
影响因子：
--
通讯作者：
Ryter SW
中科院分区：
文献类型：
--
作者：
Choi AJ;Ryter SW
自噬通过溶酶体依赖性降解途径提供细胞器和蛋白质周转的机制。在饥饿过程中，自噬发挥稳态功能，通过回收代谢前体促进细胞存活。此外，自噬可以与其他重要过程相互作用，如程序性细胞死亡，炎症和适应性免疫机制，从而可能影响疾病的发病机制。自噬蛋白缺乏的巨噬细胞显示出增强的半胱天冬酶-1依赖性促炎细胞因子产生和炎性体的激活。自噬通过促进细胞内细菌清除在感染性疾病和脓毒症中提供功能性作用。自噬相关基因突变导致自噬功能丧失，与克罗恩病的发病机制有关。此外，自噬依赖性机制已被提出在涉及炎症的几种肺部疾病的发病机制中，包括囊性纤维化和肺动脉高压。旨在调节自噬的策略可能会导致与炎症相关的疾病的治疗干预。
Autophagy provides a mechanism for the turnover of cellular organelles and proteins through a lysosome-dependent degradation pathway. During starvation, autophagy exerts a homeostatic function that promotes cell survival by recycling metabolic precursors. Additionally, autophagy can interact with other vital processes such as programmed cell death, inflammation, and adaptive immune mechanisms, and thereby potentially influence disease pathogenesis. Macrophages deficient in autophagic proteins display enhanced caspase-1-dependent proinflammatory cytokine production and the activation of the inflammasome. Autophagy provides a functional role in infectious diseases and sepsis by promoting intracellular bacterial clearance. Mutations in autophagy-related genes, leading to loss of autophagic function, have been implicated in the pathogenesis of Crohn's disease. Furthermore, autophagy-dependent mechanisms have been proposed in the pathogenesis of several pulmonary diseases that involve inflammation, including cystic fibrosis and pulmonary hypertension. Strategies aimed at modulating autophagy may lead to therapeutic interventions for diseases associated with inflammation.