Marcos G. Teneche

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 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 identifies SAA1-TLR4 signaling as a tumor-derived pathway driving muscle wasting in pancreatic cancer, showing that targeting this pathway can preserve muscle mass and improve survival without affecting tumor growth.

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.

CHASM detects chromosomal copy number alterations in single-cell data, revealing age-related genomic instability in specific cell types and states.

The paper identifies a widespread transcript leakage issue in spatial transcriptomics and introduces DeLeakage, a Bayesian method that improves data cleaning and cell-type annotation.

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.

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

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.