Local infusion of bicarbonate into hepatocellular carcinoma markedly enhances local tumor control by transarterial chemoembolization.

A non-canonical p53 function in adipocyte plays a critical role in energy homeostasis and is involved in obesity-associated metabolic dysfunctions.

The MondoA transcription factor localizes to the outer mitochondrial membrane where it coordinates an adaptive transcriptional response to elevated cellular energy represented by high cytoplasmic glucose and high mitochondrial ATP.

An interaction between the ion channel ASIC1a and the protein RIP1 is responsible for neuronal death caused by tissue acidosis.

Integrative multi-omics reveals global dysregulation in hepatic metabolism during prolonged sepsis.

Exercise can induce metabolic changes that strikingly impact cytotoxic T cell function and in turn affect cancer progression.

Building on previous work (Guarani et al., 2015), MICOS (mitochondrial contact site) assembly and cristae junction formation are shown to have a critical role in human health.

A revertible Leigh Syndrome French Canadian Type (LSFC) disease model recapitulates the clinical phenotypes which can be rescued using a liver-specific genetic model therapy.

Identifying 1,907 mitochondrial somatic mutations from 1,675 tumor tissues provides new insights into the causes and effects of the mitochondrial genome mutations found in human cancers.

Cryo-EM structure of the mammalian respiratory supercomplex containing complexes I, III and IV shows a functional asymmetry of complex III, providing strong evidence for directed electron flow in the respirasome.