Energy metabolism articles from across Nature Portfolio

This Review discusses the role of mitophagy in cellular and organismal health and disease, with a specific focus on human ageing and evidence obtained in clinical studies.

Neuronal somata perform higher levels of aerobic glycolysis and lower levels of OXPHOS than terminals, which safeguards against oxidative damage.

The immune suppression required for the resolution of acute inflammation is characterised by molecular and metabolic reprogramming of myeloid cells. Authors here show that the transcription factor ZEB1 is a key mediator of the pathway governing transition from inflammation to immunosuppression via regulating mitochondrial translation in macrophages.

The mechanisms by which mitochondria are transferred between cells and how intercellular mitochondria transfer regulates physiological processes and disease pathogenesis are discussed.

Impaired tricarboxylic acid cycle and oxidative phosphorylation cause reduced energy content in neurons upon neuroinflammation and contribute to axonal degeneration in multiple sclerosis.

Mitochondria are dynamic organelles, changing their morphology and functional capacity in response to physiological and metabolic cues. A study uncovers a role for the typically nutrient-responsive mTORC2 during fasting in vivo to promote mitochondrial fission via the activation of a signalling pathway that involves NDRG1 and CDC42.