In addition to increasing glycolysis, some proliferating cells exhibiting the Warburg effect also increase oxidative phosphorylation through mitochondrial fusion.

Mitochondrial fusion enables a metabolic transition during spermatogenesis.

The cancer testis antigen COX6B2 enhances cytochrome c oxidase activity thereby promoting proliferation and survival in cancer cells and represents a therapeutic target for inhibiting oxidative phosphorylation selectively in tumors.

Parasitic lineages of Rozellomycota are shaped by repeated and independent gene losses.

Exosomes from cancer-associated fibroblasts enhance the "Warburg effect" in tumors and contain de novo metabolites that can contribute to the entire compendia of central carbon metabolism within cancer cells.

Biochemical analyses show that mitochondrial COX16 assists in the process of copper insertion into COX2 and reveal a second COX16 function in linking assembly routes of the redox center-containing COX1 and COX2 subunits.

Changes in pathways of lipid oxidation, glycolysis, and mitochondrial oxidative phosphorylation are common strategies to cope with high-altitude hypoxia, but some changes require longer evolutionary time to arise.

The shutoff of aerobic glycolysis in neuronal differentiation is essential for neuronal survival.

Mitochondrial-targeted SS-31 peptide ameliorates mitochondrial dysfunction and rescues pre-existing cardiac dysfunction in old mice, supporting the translational potential of mitochondrial protective interventions to treat age-related diseases.

Long-term exposure to recipient's alloantigens promotes major metabolic defects in T cells that are independent of PD-1-mediated regulation.