What is it about?
Neuroinflammation is associated with many neurodegenerative diseases such as Alzheimer’s disease and multiple sclerosis (MS). Thus, decreasing neuroinflammation may be a promising treatment for these diseases. Apoptosis signalrelated kinase 1 (ASK1) has been shown to cause neuroinflammation in neurodegenerative disease models, but its mechanism of action has been unclear. Here, we generated conditional knockout mice that lack ASK1 in T cells, dendritic cells, microglia/macrophages, microglia, or astrocytes, to assess the roles of ASK1 during experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. We propose that ASK1 is required in microglia and astrocytes to cause and maintain neuroinflammation by a feedback loop between these two cell types.
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Why is it important?
Our findings demonstrate cell-type–specific roles of ASK1 and suggest phase-specific ASK1-dependent glial cell interactions in EAE pathophysiology.
Perspectives
It has been quite a long time since we published our ASK1 work in EMBO Molecular Medicine, I am grateful to all the supports that I received during this period of time.
Dr. Xiaoli Guo
Read the Original
This page is a summary of: ASK1 signaling regulates phase-specific glial interactions during neuroinflammation, Proceedings of the National Academy of Sciences, January 2022, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2103812119.
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