Revealing YBR238C's involvement in the TORC1–mitochondria feedback loop deepens our understanding of aging biology, emphasizing the TOMITO concept as a crucial mechanism in cellular aging regulation.

Cross-sectional transcriptome analysis of mice, covering the whole lifespan, reveals that inter-tissue divergence during development is accompanied by a weaker but widespread convergence during ageing.

Aging is associated with stress-induced senescence of adipose stromal cells, leading to impaired adipogenesis, oxidative stress, mitochondrial dysfunction, and insulin resistance, all being alleviated by metformin treatment of adipose stromal cells.

An increase in transcriptional noise generally assumed to characterize aged cells and tissues is shown to derive instead from technical and biological issues that underlie single-cell RNA sequencing experiments.

Although cellular organelles show a functional deterioration in aging, genetic loci associated with common age-associated disease instead nominate nuclear transcription factors across several age-related diseases.

In mitotically aging yeast cells, the cytosol acidifies, the distances between the organellar membranes decrease dramatically, but crowding on the scale of the average size protein is relatively stable.

Protons are pumped out of mother cells by a protein that accumulates over time and this leads to cellular aging, but this protein is largely absent from daughter cells, which mediates rejuvenation.

Partial ablation of osteocytes alters lineage cell specifications in bone and bone marrow, resulting in the acceleration of skeletal aging.

With replicative age, S. cerevisiae shifts from a fermentative towards an unusual respiratory metabolism, accompanied by a decrease in growth and glucose uptake rate.

The use of forward genetic screens in zebrafish identifies a new model of vertebrate aging, defining the regulating of the onset of aging phenotypes through maintenance of progenitor cell populations.