IL-4 activates ULK1/Atg9a/Rab9 in asthma, NLRP3 inflammasomes, and Golgi fragmentation by increasing autophagy flux and mitochondrial oxidative stress-Reference-Cited by-同舟云学术

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IL-4 activates ULK1/Atg9a/Rab9 in asthma, NLRP3 inflammasomes, and Golgi fragmentation by increasing autophagy flux and mitochondrial oxidative stress

Published:2024-05 Issue: Volume:71 Page:103090
ISSN:2213-2317
Container-title:Redox Biology
language:en
Short-container-title:Redox Biology

Author:

Xu Chang,Song Yilan,Liu Wanting,Liu Ruobai,Bai Qiaoyun,Li Liangchang,Wang Chongyang,Yan Guanghai^ORCID

Funder

Yanbian University

National Natural Science Foundation of China

Publisher

Elsevier BV

Reference33 articles.

1. Trends in worldwide asthma prevalence;Asher;Eur. Respir. J.,2020

2. Distinct spatial and temporal roles for Th1, Th2, and Th17 cells in asthma;Luo;Front. Immunol.,2022

3. Anti-interleukin-13 and anti-interleukin-4 agents versus placebo, anti-interleukin-5 or anti-immunoglobulin-E agents, for people with asthma;Gallagher;Cochrane Database Syst. Rev.,2021

4. Acetylation in the regulation of autophagy;Xu;Autophagy,2023

5. p38 MAPK inhibits autophagy and promotes microglial inflammatory responses by phosphorylating ULK1;He;J. Cell Biol.,2018

Cited by 1 articles. 订阅此论文施引文献订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献

1. Unraveling the role of NLRP3 inflammasome in allergic inflammation: implications for novel therapies;Frontiers in Immunology;2024-07-26

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