The metabolic ER stress sensor IRE1 alpha suppresses alternative activation of macrophages and impairs energy expenditure in obesity
文献类型：期刊论文
| 作者 | Shan, Bo6; Wang, Xiaoxia6; Wu, Ying6; Dai, Jianli6; Zhao, Feng6; He, Shengqi6; Duan, Sheng-Zhong6; Xu, Chi7; Han, Jing-Dong J.7; Xia, Zhixiong8 |
| 刊名 | NATURE IMMUNOLOGY
 |
| 出版日期 | 2017 |
| 卷号 | 18期号:5页码:519-529 |
| ISSN号 | 1529-2908 |
| DOI | 10.1038/ni.3709 |
| 文献子类 | Article |
| 英文摘要 | Obesity is associated with metabolic inflammation and endoplasmic reticulum (ER) stress, both of which promote metabolic disease progression. Adipose tissue macrophages (ATMs) are key players orchestrating metabolic inflammation, and ER stress enhances macrophage activation. However, whether ER stress pathways underlie ATM regulation of energy homeostasis remains unclear. Here, we identified inositol-requiring enzyme 1 alpha (IRE1 alpha) as a critical switch governing M1-M2 macrophage polarization and energy balance. Myeloid-specific IRE1 alpha abrogation in Ern1(f/f); Lyz2-Cre mice largely reversed high-fat diet (HFD)-induced M1-M2 imbalance in white adipose tissue (WAT) and blocked HFD-induced obesity, insulin resistance, hyperlipidemia and hepatic steatosis. Brown adipose tissue (BAT) activity, WAT browning and energy expenditure were significantly higher in Ern1(f/f); Lyz2-Cre mice. Furthermore, IRE1 alpha ablation augmented M2 polarization of macrophages in a cell-autonomous manner. Thus, IRE1 alpha senses protein unfolding and metabolic and immunological states, and consequently guides ATM polarization. The macrophage IRE1 alpha pathway drives obesity and metabolic syndrome through impairing BAT activity and WAT browning. |
| 学科主题 | Immunology |
| WOS关键词 | UNFOLDED PROTEIN RESPONSE ; ENDOPLASMIC-RETICULUM ; ADIPOSE-TISSUE ; BEIGE FAT ; POLARIZATION ; DISEASE ; INSULIN ; CELL ; THERMOGENESIS ; INFLAMMATION |
| 语种 | 英语 |
| WOS记录号 | WOS:000399378700009 |
| 出版者 | NATURE PUBLISHING GROUP |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/822]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所 |
| 作者单位 | 1.Wuhan Univ, Inst Adv Studies, Coll Life Sci, Hubei Key Lab Cell Homeostasis, Wuhan, Peoples R China; 2.Shanghai Jiao Tong Univ, Affiliated Peoples Hosp 6, Shanghai Diabet Inst,Shanghai Key Lab Diabet Mell, Shanghai Clin Ctr Diabet,Dept Endocrinol & Metab, Shanghai, Peoples R China; 3.Chinese Acad Sci, Shanghai Inst Mat Med, Natl Ctr Drug Screening, Shanghai, Peoples R China; 4.Peking Univ, Beijing Key Lab Cardiometab Mol Med, Acad Adv Interdisciplinary Studies, Inst Mol Med,Peking Tsinghua Ctr Life Sci, Beijing, Peoples R China; 5.Univ Michigan, Med Sch, Dept Mol & Integrat Physiol, Ann Arbor, MI 48109 USA, 6.Univ Chinese Acad Sci, Chinese Acad Sci, Shanghai Inst Biol Sci, Key Lab Nutr & Metab,Inst Nutr Sci, Shanghai, Peoples R China; 7.Chinese Acad Sci, Shanghai Inst Biol Sci, Key Lab Computat Biol, Chinese Acad Sci Max Planck Partner Inst Computat, Shanghai, Peoples R China; 8.Huazhong Univ Sci & Technol, Minist Educ, Key Lab Mol Biophys, Cellular Signaling Lab, Wuhan, Peoples R China; 9.Univ Texas Southwestern Med Ctr Dallas, Dept Internal Med, Touchstone Diabet Ctr, Dallas, TX 75390 USA; |
| 推荐引用方式 GB/T 7714 | Shan, Bo,Wang, Xiaoxia,Wu, Ying,et al. The metabolic ER stress sensor IRE1 alpha suppresses alternative activation of macrophages and impairs energy expenditure in obesity[J]. NATURE IMMUNOLOGY,2017,18(5):519-529. |
| APA | Shan, Bo.,Wang, Xiaoxia.,Wu, Ying.,Dai, Jianli.,Zhao, Feng.,...&,.(2017).The metabolic ER stress sensor IRE1 alpha suppresses alternative activation of macrophages and impairs energy expenditure in obesity.NATURE IMMUNOLOGY,18(5),519-529. |
| MLA | Shan, Bo,et al."The metabolic ER stress sensor IRE1 alpha suppresses alternative activation of macrophages and impairs energy expenditure in obesity".NATURE IMMUNOLOGY 18.5(2017):519-529. |
入库方式： OAI收割
来源：上海营养与健康研究所
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