Methylation pace of aging is a novel measure requiring only a blood sample that clinical-trial and observational studies can use to test if treatments modify how fast participants are aging.

A comprehensive mapping of the proteome and transcriptome during the complete replicative lifespan of budding yeast predicted an increased abundance of the protein biogenesis machinery is most causal for aging.

Resetting a young gut microbiota in middle-aged individuals extends life span and slows aging in the naturally short-lived turquoise killifish, a new vertebrate model organism to study how the microbiota affects the aging process.

Modulation of histone levels in gut enterocytes by rapamycin treatment alters chromatin organisation and induces intestinal autophagy through transcriptional regulation to prevent age-related decline in the intestine and extend lifespan.

Ketogenic diet protects against coronavirus-infected aged mice, which, like humans, are significantly more susceptible to infections, by deactivating NLRP3 inflammasome, reducing pathogenic monotypes, and expanding γδ T cells in the lung.

Muscle stem cells locally respond to perturbations of motor neurons and the neuromuscular junction.

The first epigenetic clock for rats was developed and revealed to reflect phenotypic aging and captured the effects of longevity interventions.

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.

Direct reprogramming of smooth muscle cells from HGPS patients revealed that BMP4 is a key contributor of vascular degeneration and might represent a new therapeutic target.

Autophagic flux assays in the nematode Caenorhabditis elegans suggest that autophagy decreases during normal aging, whereas long-lived daf-2 and glp-1 mutants maintain autophagic capacity in distinct spatiotemporal-specific manners to extend lifespan.