Aaron P. Havas

This study identifies age-associated repression of HNF4α as a driver of liver metabolic dysfunction and shows that restoring HNF4α can reverse some age-related liver defects.

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

This study shows that aging-induced CD44 in hepatocytes activates the IL6/JAK/STAT3 pathway, leading to impaired T cell function in the liver.

This study shows that cellular senescence disrupts liver zonation and hepatocyte function with age by altering gene expression and cell signaling.

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

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.

The paper investigates how enhancer interactomes reconfigure during senescence and aging, identifying hyper-connected enhancer communities linked to gene expression and potential therapeutic targets.

The paper introduces ImAge, an image-based biomarker of aging and rejuvenation using chromatin and epigenetic patterns, showing correlation with chronological age and response to interventions.