Mitochondrial dysfunctions in T cells: focus on inflammatory bowel disease

Mitochondria has emerged as a critical ruler of metabolic reprogramming in immune responses and inflammation. In the context colitogenic T cells IBD, there been increasing research interest pathways glycolysis, pyruvate oxidation, glutaminolysis. These have shown to play crucial role cells, leading increased inflammatory cytokine production tissue damage. addition reprogramming, mitochondrial dysfunction also implicated pathogenesis IBD. Studies that exhibit impaired respiration, elevated levels mROS, alterations calcium homeostasis, biogenesis, aberrant mitochondria-associated membrane formation. Here, we discuss our current knowledge dysfunctions well potential therapeutic applications for treating IBD with evidence from animal experiments.