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Conditional deletion of the mitochondrial transcription factor A (Tfam) in CD4 + T cells led to an imbalance in the NAD + /NADH ratio of mitochondria, which induced metabolic reprogramming toward glycolysis and thereby contributed to their pro-inflammatory phenotype, consequently exacerbating the in vivo immune response

Abstract Background: Glutathione (GSH) metabolism supports tumor redox balance and drug resistance, while long non-coding RNAs (lncRNAs) influence lung adenocarcinoma (LUAD) progression

However, the lack of oxygen and substrates generally keeps ROS generation relatively lower compared to the subsequent phase

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