Xiao Dong

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

This study identifies organized vulnerability in the aging genome, showing that certain genes and pathways are less mutated while others accumulate more mutations, suggesting a network-based mechanism for cellular decline.

The paper analyzes transcriptomic changes in human fibroblasts under different senescence-inducing conditions, finding shared pathway-level responses and inducer-specific gene-level variations.

The paper identifies age-related increases in inter-individual gene expression variability using the Gene Stability Score in GTEx data, showing distinct biological impacts and non-random network architecture.

STEVE evaluates cell-type annotation robustness in scRNA-seq datasets through subsampling, novel cell detection, and benchmarking against ground-truth labels.

MCAREDB integrates scRNA-seq datasets from mouse cardiac regeneration studies to enable comparative analysis of gene expression and pathways across developmental and injury contexts.

SomaMutDB 2.0 is a database that catalogs 8.9 million somatic mutations from 10,852 samples and provides functional annotations to assess their impact in normal human tissues.

This study analyzes somatic mutations in chondrocytes from aging and osteoarthritis patients using single-cell whole genome sequencing, finding age-related mutation accumulation with a lower rate in OA chondrocytes.

The paper benchmarks somatic mutation detection in noncancerous cells using single-cell and single-molecule whole-genome sequencing to assess platform-specific biases and their impact on mutation detection.

This study identifies fucoidans as senotherapeutics that enhance SIRT6-dependent DNA repair and reduce senescence in aged mice.

This paper introduces SMM-SV-seq, a method to detect rare somatic structural-variant breakpoints in bulk DNA with high precision and recall, validated using human and Drosophila DNA mixtures and clinical treatments.

This study shows that DNA mismatch repair-deficient mouse fibroblasts can tolerate high mutation burdens in vitro without significant growth effects, revealing mutation-driven population changes and negative selection.

The paper shows that human fibroblasts undergo negative selection against harmful mutations, maintaining growth despite high mutation loads.

This study uses single-cell whole-genome sequencing to compare mutation burdens in early passage and deeply senescent human fibroblasts, finding increased single-nucleotide variations and aneuploidies in senescent cells.

SCCNV identifies copy number variations from single-cell whole-genome sequencing data by adjusting for amplification bias.

The paper shows that somatic mutation frequencies increase with age in human liver hepatocytes but are lower in liver stem cells and organoids.

This study uses single-cell whole-genome sequencing to analyze mutational landscapes in Msh2-deficient mouse fibroblasts, revealing elevated SNVs and INDELs with distinct mutational signatures.

This study uses single-cell whole-genome sequencing to analyze somatic mutations in B lymphocytes across the human lifespan, finding age-related mutation accumulation and potential cancer-related events.

The paper identifies rare spontaneous retrotranspositions in normal human tissues, showing cell-type-specific variation and association with differentiation processes.