To promote longevity under heat stress shares yeast aging factors with progeny through a down-regulation of the diffusion barrier in the membranes between the mitotic cells.
Epigenetic drift of H3K27me3 is one of the molecular mechanisms that contribute to aging, and stimulation of glycolysis promotes metabolic health and longevity.
Two SET-domain containing proteins regulate H3K4me3 by their binding to H3K4me3 through their PHD domain and directly regulate expression of a subset of genes.
Genetic analysis reveals NADPH oxidase generated reactive oxygen species as signals to re-establish cellular homeostasis during aging via activating a transcriptional response.
A mouse model reveals that a p53 SNP impacts longevity via modulating the balance of cancer risk and the self-renewal function of stem/progenitor cells, which supports a role of p53 in regulation of longevity.
Profiling of fibroblasts across mammals captures differences in longevity at the level of global gene expression and metabolite levels and reveals pathways that define these differences.
Chronic and excessive inflammation can lead to exhaustion of the supply of hematopoietic stem cells and to myeloid malignancies in mice, mimicking important aspects of the myelodysplastic syndrome found in humans.
Directly targeting the ribosome to attenuate translation partly mimics the integrated stress response, increasing lifespan and preserving protein folding capacity even in older individuals with dysfunctional stress response signaling.
