Mutations affecting a nuclear encoded metalloprotease cause of a new form of mitochondriopathy, highlighting the importance of this protease for mitochondrial function in humans.

Compounds that activate integrated stress response kinases inhibit mitochondrial fragmentation induced by chemical or genetic insults, indicating that targeting this pathway offers opportunities to mitigate mitochondrial fragmentation in diverse diseases.

A trial of mitofusin activation shows neuron regeneration and phenotype reversal in vitro and in vivo in experimental Charcot–Marie–Tooth disease type 2A caused by mitofusin 2 mutations.

A comprehensive analysis of the human MICOS complex has identified a novel subunit called QIL1 that is required for cristae junction formation in human cells and Drosophila, through its role in the assembly of the MICOS complex.

Novel transgenic zebrafish lines allow selective ablation of neuronal mitochondria by far red light, providing a powerful tool for investigating mitochondrial homeostasis in neurons and mitochondrial mechanisms in neurological disease.

Light controls can fine tune microbiome–host interaction to qualitatively regulate host longevity with temporal and spatial precision.

Axon degeneration occurs via an ordered sequence of events downstream of SARM1 that proceeds from ATP loss, to defects in mitochondrial movement and depolarization, followed by calcium influx, phosphatidylserine externalization, loss of membrane permeability, and ending with catastrophic axonal self-destruction.

An extracellular modulator of IGF1 signaling, Pappaa, regulates endoplasmic reticulum–mitochondria connections, which are critical for metabolic homeostasis and hair cell survival.

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

Drosophila HNF4 directs a developmental switch at the onset of adulthood that suppresses diabetes by promoting mitochondrial function and supporting glucose-stimulated insulin secretion.