Complement:a global immunometabolic regulator in amyotrophic lateral sclerosis

作     者：Martin W.Lo John D.Lee Martin W.Lo;John D.Lee

作者机构：School of Biomedical SciencesFaculty of MedicineThe University of QueenslandSt LuciaQueenslandAustralia 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2021年第16卷第6期

页      面：1210-1211页

核心收录：

学科分类：0710[理学-生物学] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100204[医学-神经病学] 10[医学] 

基　　金：support from Motor Neuron Disease Research Institute of Australia(Grant Award Number:GIA1930 and PDF1604) 

主　　题：inflammation metabolism elevated 

摘      要：Recently,McDonald et al.(2020)proposed that complement causes a metabolic switch to lipid consumption in amyotrophic lateral sclerosis(ALS),which raises the possibility of complement as a global immunometabolic *** ALS,neuromuscular degeneration occurs concurrently with complement-mediated inflammation,glucose intolerance,and elevated lipid ***,complement is being increasingly recognized as a metabolic regulator that can induce insulin resistance and alter fuel source ***,the authors propose that chronic complement activation may be driving metabolic reprogramming in ALS,which has broad implications for the field of immunometabolism and would be the first mechanistic explanation of the“lipid switchin ***,it suggests that complement can drive a global shift in resources during inflammation,in which glucose is redirected from peripheral tissues to immune cells to support their inflammatory actions.