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- W4386962011 abstract "Mitochondria has emerged as a critical ruler of metabolic reprogramming in immune responses and inflammation. In the context of colitogenic T cells and IBD, there has been increasing research interest in the metabolic pathways of glycolysis, pyruvate oxidation, and glutaminolysis. These pathways have been shown to play a crucial role in the metabolic reprogramming of colitogenic T cells, leading to increased inflammatory cytokine production and tissue damage. In addition to metabolic reprogramming, mitochondrial dysfunction has also been implicated in the pathogenesis of IBD. Studies have shown that colitogenic T cells exhibit impaired mitochondrial respiration, elevated levels of mROS, alterations in calcium homeostasis, impaired mitochondrial biogenesis, and aberrant mitochondria-associated membrane formation. Here, we discuss our current knowledge of the metabolic reprogramming and mitochondrial dysfunctions in colitogenic T cells, as well as the potential therapeutic applications for treating IBD with evidence from animal experiments." @default.
- W4386962011 created "2023-09-23" @default.
- W4386962011 creator A5020512513 @default.
- W4386962011 creator A5047291248 @default.
- W4386962011 creator A5053397565 @default.
- W4386962011 date "2023-09-22" @default.
- W4386962011 modified "2023-10-11" @default.
- W4386962011 title "Mitochondrial dysfunctions in T cells: focus on inflammatory bowel disease" @default.
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