Metabolic switches between oxidative phosphorylation and aerobic glycolysis plus glutaminolysis direct T cell function by altering the flux of glucose and glutamine to N-glycosylation.

Combination of glutaminase inhibitor CB-839 and ASCT2 inhibitor V-9302 showed efficient antitumor effect against glutamine addicted liver cancer cells via glutathione depletion and reactive oxygen species (ROS) induction.

Acute myocardial infarction patient-derived endothelial cells display a strong mitochondrial proton coupling with excess ROS production, enhanced glutamine metabolism and a carbon source switch from glucose to glutamine.

Metabolic reprogramming in suppressing oxidative stress during TH17 cell differentiation.

Genetic analyses and biochemical studies show that JMJD6 promotes MYC-mediated transformation and is required for neuroblastoma growth by complexing with pre-mRNA splicing factors.

Type 2 cytokines induce macrophage innate training, where enhanced pro-inflammatory responses are fuelled by oxidative phosphorylation rather than aerobic glycolysis.

Pembrolizumab activates innate immune metabolism and function in primary human non-small cell lung cancer, whereas Pembrolizumab and beta-glucan synergize in enhancing immune metabolism and tumoridical action in brain-metastasized lung cancer.

The interplay of the host metabolic reprogramming, its negative association with antiviral biological signaling pathways and the IFN-mediated host antiviral mechanism during Crimean–Congo hemorrhagic fever orthonairovirus (CCHFV) infection could provide attractive options for therapeutic intervention of CCHF.

Iron derived from autophagy-mediated ferritin degradation in response to pressure overload induces lipid peroxidation, necrotic cardiomyocyte death, and heart failure in mice.

Editors' Summary: This Replication Study has reproduced important parts of the original paper.