When neurons are stimulated, calcium entry into mitochondria upregulates mitochondrial energy production, but glycolytic energy production in the cytosol is stimulated by elevated energy demand, not Ca²⁺ signaling.

Pyruvate and related metabolites are linked to reduced glaucoma risk among genetically predisposed individuals and mitigate disease in a mouse model, highlighting a potential metabolic mechanism of resilience.

Multi-omic analyses reveal a connection between the integrated stress response and the regulation of redox and amino acid metabolism when the TCA cycle is impaired.

Aminoglycoside tolerance in tricarboxylic acid cycle and electron transport chain mutants does not result from impaired proton motive force and altered drug uptake, but rather from the downregulation of ribosomal proteins, which are primary targets of this drug class.

The dual function of an ancient prokaryotic enzyme, which is linked to specific metabolite signals, may have been the evolutionary driving force behind its dual localization in eukaryotes.

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

Volatile anesthetics impair hepatic tricarboxylic acid cycle function in adult and neonatal mice, with citrate accumulation driving a neonate-specific inhibition of beta-oxidation and ketosis through their increased relative sensitivity to malonyl-CoA.

SDH-null cancer cells decrease mitochondrial complex I to drive rewired aspartate synthesis through reductive carboxylation and pyruvate carboxylase, supporting cell proliferation and tumor growth.

Metabolic defects following expression of Aβ1-42 in nematode neurons are partially caused by inactivation of alpha-ketoglutarate dehydrogenase and can be rescued by Metformin.