Xue Lei

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 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 increasing ACSS2 levels protects neurons from age-related and tau-induced decline by enhancing synaptic and longevity gene expression.

This study shows senescent cells release chromatin components via extracellular particles, activating inflammation in neighboring cells and being present in aged mice.

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.

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

This study uses a minimal model and ACME method to show that Cro2 binding at OR3 and CI2 at OR1 affect lysogeny stability during prophage induction.

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.

SPRI predicts the pathogenicity of missense variants and identifies spatially organized mutational clusters linked to cancer and Mendelian diseases.

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