4.6 Review

Autophagy limits activation of the inflammasomes

期刊

IMMUNOLOGICAL REVIEWS
卷 281, 期 1, 页码 62-73

出版社

WILEY
DOI: 10.1111/imr.12613

关键词

cytokines; endotoxin shock; inflammation; inflammatory bowel disease; signaling proteins; toll-like receptors/pattern recognition receptors

资金

  1. Japan Society for the Promotion of Science [26713005]
  2. Ministry of Education, Culture, Sports, Science and Technology [17H06415]
  3. Japan Agency for Medical Research and Development-Core Research for Evolutional Science and Technology
  4. Grants-in-Aid for Scientific Research [17H06413] Funding Source: KAKEN

向作者/读者索取更多资源

Inflammasomes are multiprotein complexes that control the maturation and production of interleukin-1 family members and play crucial roles in host defense against pathogens. However, dysregulated activation of inflammasomes is associated with intense inflammation, leading to the development of inflammatory diseases. Therefore, inflammasomes must be activated at a proper strength to protect against infection and avoid tissue damage. Recent studies have highlighted the cross-talk between inflammasome activation and autophagy, the cellular machinery associated with the degradation of intracellular components and maintenance of cellular homeostasis. Notably, deficiencies in autophagy-related proteins induce the aberrant activation of inflammasomes, causing severe tissue damage. In contrast, autophagy inducers ameliorate symptoms of inflammasome-related diseases. In this review, we discuss recent advances in the involvement of autophagy in regulating inflammasomes activation and in the development of inflammatory diseases.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据