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.

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

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

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.

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.

Cell-wide Ca²⁺ signals that regulate numerous cellular functions comprise dual Ca²⁺ release modes through IP₃ receptors, punctate transients mediated by clustered receptors and spatiotemporally diffuse release through functionally distinct receptors.

In neuronal mitophagy, Parkin and OPTN induce efficient sequestration of damaged somal mitochondria into autophagosomes, but slow turnover via lysosomal acidification may be a point of vulnerability for the cell.

Silencing the acyl-coA synthethase ACSL1 protects against saturated fat lipotoxicity by preventing the degradation of polyunsaturated fatty acids, allowing them to be incorporated into phospholipids and improves membrane fluidity.

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