Rouven Arnold

Age-associated repression of HNF4α is a driver and potential therapeutic target in liver metabolic dysfunction

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.

Targeting CyclinD1-CDK6 to Mitigate Senescence-Driven Inflammation and Age-Associated Functional Decline

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

Aging-induced hepatocyte CD44 drives IL6/STAT3 signaling and associates with impaired neighboring T cell function.

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

NAMPT activation uncovers a senescence-specific vulnerability and promotes healthy aging in combination with NAM

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

HIRA-mediated H3.3 deposition preserves hepatocyte cell identity during liver aging

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.

Aging alters tumor cell - T cell crosstalk to promote breast cancer progression

This study shows that aging reduces T cell recruitment in breast cancer by decreasing Cxcl9/Cxcl10 expression in tumor cells, leading to weakened anti-tumor immunity.

Nucleosome stability safeguards cell identity, stress resilience and healthy aging

The paper shows that reduced nucleosome stability impairs cell identity, stress resilience, and healthy aging across species.

Inactivation of histone chaperone HIRA unmasks a link between normal embryonic development of melanoblasts and maintenance of adult melanocyte stem cells

This study shows that inactivating HIRA during embryonic development affects melanoblasts and leads to aging-related defects in melanocyte stem cells, but not in postnatal melanocytes.