Karl N. Miller

This paper introduces a measure of transcriptional dyscoordination to quantify aging in single cells, showing it increases with age and is linked to cellular processes like senescence and genome instability.

This study shows that targeting CCND1-CDK6 reduces DNA damage, inflammation, and age-related decline in mice by suppressing SASP and ISG expression.

This paper identifies a strategy combining NAMPT activation and NAM supplementation to target NAD+ dysregulation and senescent cells, promoting healthy aging in mice.

This study shows that a H2A.Z mutant reduces the senescence-associated secretory phenotype in human fibroblasts without affecting cell cycle genes.

This study shows that HIRA-mediated H3.3 deposition maintains hepatocyte identity during aging, and its loss leads to metabolic dysfunction and fibrosis, which can be partially reversed by tissue regeneration.

This study shows that rapamycin reduces age-related liver damage caused by a high-fat diet in mice by reversing transcriptional changes and metabolic dysfunction.

This study shows that aged livers have heightened interferon signaling that suppresses cancer but also has harmful effects, leading to a 'precarious balance' in tumor development.

This study identifies a mitochondria-regulated p53 circuit that links genomic instability and inflammation in senescent cells, showing p53 suppresses inflammation without affecting cell cycle arrest.