Autophagy-activating strategies to promote innate defense against mycobacteria.,Experimental & Molecular Medicine

当前位置： X-MOL 学术 › Exp. Mol. Med. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

Autophagy-activating strategies to promote innate defense against mycobacteria.
Experimental & Molecular Medicine ( IF 9.5 ) Pub Date : 2019-12-11 , DOI: 10.1038/s12276-019-0290-7
Yi Sak Kim _{1,

2} , Prashanta Silwal _{1,

2} , Soo Yeon Kim ₃ , Tamotsu Yoshimori _{4,

5} , Eun-Kyeong Jo _{1,

2,

6}

Affiliation

Mycobacterium tuberculosis (Mtb) is a major causal pathogen of human tuberculosis (TB), which is a serious health burden worldwide. The demand for the development of an innovative therapeutic strategy to treat TB is high due to drug-resistant forms of TB. Autophagy is a cell-autonomous host defense mechanism by which intracytoplasmic cargos can be delivered and then destroyed in lysosomes. Previous studies have reported that autophagy-activating agents and small molecules may be beneficial in restricting intracellular Mtb infection, even with multidrug-resistant Mtb strains. Recent studies have revealed the essential roles of host nuclear receptors (NRs) in the activation of the host defense through antibacterial autophagy against Mtb infection. In particular, we discuss the function of estrogen-related receptor (ERR) α and peroxisome proliferator-activated receptor (PPAR) α in autophagy regulation to improve host defenses against Mtb infection. Despite promising findings relating to the antitubercular effects of various agents, our understanding of the molecular mechanism by which autophagy-activating agents suppress intracellular Mtb in vitro and in vivo is lacking. An improved understanding of the antibacterial autophagic mechanisms in the innate host defense will eventually lead to the development of new therapeutic strategies for human TB.

中文翻译：

促进对分枝杆菌的先天防御的自噬激活策略。

结核分枝杆菌 (Mtb) 是人类结核病 (TB) 的主要致病病原体，是世界范围内严重的健康负担。由于结核病的耐药形式，对开发治疗结核病的创新治疗策略的需求很高。自噬是一种细胞自主的宿主防御机制，通过该机制，细胞质内的货物可以被传递，然后在溶酶体中被破坏。以前的研究报告说，自噬激活剂和小分子可能有助于限制细胞内 Mtb 感染，即使是耐多药 Mtb 菌株也是如此。最近的研究揭示了宿主核受体 (NRs) 在通过针对 Mtb 感染的抗菌自噬激活宿主防御中的重要作用。尤其，我们讨论了雌激素相关受体 (ERR) α 和过氧化物酶体增殖物激活受体 (PPAR) α 在自噬调节中的作用，以提高宿主对 Mtb 感染的防御能力。尽管与各种药物的抗结核作用有关的有希望的发现，但我们对自噬激活剂在体外和体内抑制细胞内 Mtb 的分子机制的理解仍然缺乏。对先天宿主防御中的抗菌自噬机制的更好理解最终将导致人类结核病新治疗策略的发展。我们缺乏对自噬激活剂在体外和体内抑制细胞内 Mtb 的分子机制的理解。对先天宿主防御中的抗菌自噬机制的更好理解最终将导致人类结核病新治疗策略的发展。我们缺乏对自噬激活剂在体外和体内抑制细胞内 Mtb 的分子机制的理解。对先天宿主防御中的抗菌自噬机制的更好理解最终将导致人类结核病新治疗策略的发展。

更新日期：2019-12-11

点击分享查看原文

点击收藏

公开下载

阅读更多本刊最新论文