ACSL4 promotes microglia-mediated neuroinflammation by regulating lipid metabolism and VGLL4 expression
Brain, Behavior, and Immunity, ISSN: 0889-1591, Vol: 109, Page: 331-343
2023
- 34Citations
- 23Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations34
- Citation Indexes34
- CrossRef34
- 31
- Captures23
- Readers23
- 23
Article Description
Acyl-CoA synthetase long-chain family member 4 (ACSL4) is an important isozyme in polyunsaturated fatty acid (PUFA) metabolism. The role of ACSL4 in the lipopolysaccharide (LPS)-induced inflammation of microglia, and the effects of ACSL4-mediated inflammation on the progression of Parkinson’s disease (PD) are unknown. In this study, we found that ACSL4 expression was increased after LPS stimulation. Knocking down ACSL4 in microglia decreased proinflammatory cytokine production. Mechanistically, ACSL4 reduced vestigial-like family member 4(VGLL4) expression to promote NF-κB signal transduction; and ACSL4 regulated lipid composition after LPS stimulation. In addition, knocking down ACSL4 alleviated neuroinflammation in a systemic LPS model and acute l-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP) model. These data revealed ACSL4 to be a novel regulator that promotes microglia-mediated neuroinflammation by regulating VGLL4 expression and lipid metabolism.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0889159123000375; http://dx.doi.org/10.1016/j.bbi.2023.02.012; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85148378642&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/36791893; https://linkinghub.elsevier.com/retrieve/pii/S0889159123000375; https://dx.doi.org/10.1016/j.bbi.2023.02.012
Elsevier BV
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