期刊
TRENDS IN IMMUNOLOGY
卷 42, 期 1, 页码 45-58出版社
CELL PRESS
DOI: 10.1016/j.it.2020.11.004
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资金
- National MS Society (USA) [RG-1802-30200]
- Italian Multiple Sclerosis Association (AISM) [2018/R/14]
- US Department of Defense (DoD) Congressionally Directed Medical Research Programs (CDMRP) [MS-140019]
- Bascule Charitable Trust [RG 75149, RG 98181]
- Fondazione Italiana Sclerosi Multipla (FISM) [2017/B/5]
- Addenbrooke's Charitable Trust [RG 97519]
- '5 per mille' public funding
- Wellcome Trust [220711/Z/20/Z]
- Wellcome Trust [220711/Z/20/Z] Funding Source: Wellcome Trust
The rapidly evolving field of immunometabolism has highlighted the key signaling roles of metabolites in cellular communication, with recent evidence focusing on the succinate-SUCNR1 axis as a crucial regulator of tissue homeostasis. Succinate signaling through SUCNR1 guides diverse immune cell responses, which are influenced by tissue and context. This research explores cellular pathways regulated by the succinate-SUCNR1 axis and its impact on myeloid cell function, aiming to identify new therapeutic targets for addressing detrimental myeloid cell responses in tissues, including those in the persistently inflamed central nervous system (CNS).
The rapidly evolving area of immunometabolism has shed new light on the fundamental properties of products and intermediates of cellular metabolism (metabolites), highlighting their key signaling roles in cell-to-cell communication. Recent evidence identifies the succinate-succinate receptor 1 (SUCNR1) axis as an essential regulator of tissue homeostasis. Succinate signaling via SUCNR1 guides divergent responses in immune cells, which are tissue and context dependent. Herein, we explore the main cellular pathways regulated by the succinate- SUCNR1 axis and focus on the biology of SUCNR1 and its roles influencing the function of myeloid cells. Hence, we identify new therapeutic targets and putative therapeutic approaches aimed at resolving detrimental myeloid cell responses in tissues, including those occurring in the persistently inflamed central nervous system (CNS).
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