Literature DB >> 32307753

The potential interplay between energy metabolism and innate complement activation in amyotrophic lateral sclerosis.

Tanya S McDonald1, Pamela A McCombe2,3, Trent M Woodruff1, John D Lee1,2.   

Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressing motor neuron disease without effective treatment. Although the precise mechanisms leading to ALS are yet to be determined, there is now increasing evidence implicating the defective energy metabolism and components of the innate immune complement system in the onset and progression of its motor phenotypes. This review will survey the mechanisms by which the energy metabolism and the complement system are altered during the disease progression of ALS and how it can contribute to disease. Furthermore, it will also examine how complement activation can modify the energy metabolism in metabolic disorders, in order to highlight how the complement system and energy metabolism may be linked in ALS.
© 2020 Federation of American Societies for Experimental Biology.

Entities:  

Keywords:  TCA cycle; glucose metabolism; neurodegeneration; neuroinflammation

Year:  2020        PMID: 32307753     DOI: 10.1096/fj.201901781

Source DB:  PubMed          Journal:  FASEB J        ISSN: 0892-6638            Impact factor:   5.191


  2 in total

1.  Complement: a global immunometabolic regulator in amyotrophic lateral sclerosis.

Authors:  Martin W Lo; John D Lee
Journal:  Neural Regen Res       Date:  2021-06       Impact factor: 5.135

2.  Complement membrane attack complex is an immunometabolic regulator of NLRP3 activation and IL-18 secretion in human macrophages.

Authors:  Gisela Jimenez-Duran; Joseph Kozole; Rachel Peltier-Heap; Eleanor R Dickinson; Christopher R Kwiatkowski; Francesca Zappacosta; Roland S Annan; Nicholas W Galwey; Eva-Maria Nichols; Louise K Modis; Martha Triantafilou; Kathy Triantafilou; Lee M Booty
Journal:  Front Immunol       Date:  2022-09-27       Impact factor: 8.786

  2 in total

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