AMP‐activated protein kinase (AMPK) regulates autophagy, inflammation, and immunity and contributes to osteoclastdifferentiation and function,Biology of the Cell

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AMP‐activated protein kinase (AMPK) regulates autophagy, inflammation, and immunity and contributes to osteoclastdifferentiation and function
Biology of the Cell ( IF 2.4 ) Pub Date : 2020-06-08 , DOI: 10.1111/boc.202000008
Xishuai Tong _{1,

2,

3,

4,

5} , Roman R Ganta ₂ , Zongping Liu _{1,

3,

4,

5}

Affiliation

Osteoclasts are multinucleated giant cells, responsible for bone resorption. Osteoclast differentiation and function requires a series of cytokines to remove the old bone, which coordinates with the induction of bone remodelling by osteoblast‐mediated bone formation. Studies have demonstrated that AMP‐activated protein kinase (AMPK) play a negative regulatory role in osteoclast differentiation and function. Research involving AMPK, a nutrient and energy sensor, has primarily focused on osteoclast differentiation and function; thus, its role in autophagy, inflammation and immunity remains poorly understood. Autophagy is a conservative homoeostatic mechanism of eukaryotic cells, and response to osteoclast differentiation and function; however, how it interacts with inflammation remains unclear. Additionally, based on the regulatory function of different AMPK subunits for osteoclast differentiation and function, its activation is regulated by upstream factors to perform bone metabolism. This review summarises the critical role of AMPK‐mediated autophagy, inflammation and immunity by upstream and downstream signalling during receptor activator of nuclear factor kappa‐B ligand‐induced osteoclast differentiation and function. This pathway may provide therapeutic targets for bone‐related diseases, as well as function as a biomarker for bone homoeostasis.

中文翻译：

AMP 活化蛋白激酶 (AMPK) 调节自噬、炎症和免疫，并有助于破骨细胞分化和功能

破骨细胞是多核巨细胞，负责骨吸收。破骨细胞的分化和功能需要一系列细胞因子来去除旧骨，这与成骨细胞介导的骨形成诱导骨重塑相协调。研究表明，AMP 活化蛋白激酶 (AMPK) 在破骨细胞分化和功能中发挥负调控作用。涉及 AMPK（一种营养和能量传感器）的研究主要集中在破骨细胞的分化和功能上；因此，它在自噬、炎症和免疫中的作用仍然知之甚少。自噬是真核细胞保守的稳态机制，是对破骨细胞分化和功能的反应；然而，它如何与炎症相互作用仍不清楚。此外，基于不同 AMPK 亚基对破骨细胞分化和功能的调节功能，其活化受上游因子调控，进行骨代谢。本综述总结了 AMPK 介导的自噬、炎症和免疫在核因子 kappa-B 配体受体激活剂诱导的破骨细胞分化和功能过程中通过上游和下游信号传导的关键作用。该通路可能为骨相关疾病提供治疗靶点，以及作为骨稳态的生物标志物。核因子κ-B配体受体激活剂诱导破骨细胞分化和功能过程中上游和下游信号传导的炎症和免疫。该通路可能为骨相关疾病提供治疗靶点，以及作为骨稳态的生物标志物。核因子κ-B配体受体激活剂诱导破骨细胞分化和功能过程中上游和下游信号传导的炎症和免疫。该通路可能为骨相关疾病提供治疗靶点，以及作为骨稳态的生物标志物。

更新日期：2020-06-08

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