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

Across a physiological span of ATP-free energy, leukemic mitochondria primarily consume, rather than produce, ATP.

The emerging importance of interorganellar communication is demonstrated by documentation of a feedback loop wherein peroxisome-generated metabolites affect mitochondrial ATP production and peroxisomal functions via signaling pathways requiring transmission of signals also through the cytosol and the nucleus.

Simultaneous calcium imaging and cell-attached recording in GCaMP6 transgenic mice in vivo reveals spiking-fluorescence relationship that supports more refined inference of neuronal activities from calcium imaging data.

Building on previous work (Reznik et al., 2016), independent measurements of mitochondrial genome copy number and expression indicate that several solid tumor types suppress respiratory metabolism compared to normal tissue.

Comparative -omic analyses of five knockout mouse strains with disrupted mitochondrial DNA expression at different levels provide a high quality resource of altered gene expression patterns that reveal several common secondary patophysiological changes of mitochondrial dysfunction.

Based on two independent methods, mitochondria operate at temperatures up to 15°C hotter than ambient, adjusting their heat production so as to maintain temperature in face of physiological stresses.

During infection, L. pneumophila reverses the ATP-synthase activity of the mitochondrial F_OF₁-ATPase to ATP-hydrolase activity in a type 4 secretion-dependent manner to prevent early cell death, thereby preserving its replication niche.

ATP enters the endoplasmic reticulum (ER) lumen through an SLC35B1/AXER-dependentCaATiER mechanism, and ATP usage in the ER renders 'anti-Warburg' effect by increasing ATP regeneration from OxPhos while decreasing glycolysis.

Inhibition of type I PRMTs increases the proliferation capabilities of MuSCs with altered cellular metabolism, while maintaining their stem-like properties such as self-renewal and engraftment potential.