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.

Specific human mitofusin 2 mutations induce selective upper body obesity with suppressed leptin expression and severe adipose mitochondrial dysfunction.

A phylum-specific ATP synthase subunit is needed for proper mitochondrial function and stability of the complex in Toxoplasma gondii.

AurkA is imported into mitochondria at interphase, and it induces organelle elongation and enhances ATP production when over-expressed.

The common view that the mitochondrion endowed eukaryotes with a boost in bioenergetic capacity above that in prokaryotes is inconsistent with a diversity of cellular features.

RSV's unique ability to co-opt host cell mitochondria to facilitate viral infection reveals the RSV-mitochondrial interface as a viable target for therapeutic intervention.

Mitochondrial flashes counteract the imbalance of ATP supply-and-demand and constitute an auto-regulator of ATP homeostasis in the heart.

Hemodynamic forces regulate endothelial cell metabolism, which in turn regulates endothelial inflammation.

The localization of respiratory complexes in the cell membrane emerges as a critical factor for controlling respiration in bacteria.

A genetic approach documents that mitochondrial DNA moves from donor cells to recipient mtDNA-depleted cells in whole mitochondria and that this restores mitochondrial respiration and the capacity of the cells to form tumours.