David G. Hendrickson

This study identifies declining Wnt signaling as a driver of age-related alveolar stem cell loss and shows that restoring Wnt signaling in aged mice improves lung repair but not full regeneration.

This study shows that inhibiting PTPN1/2 enhances alveolar macrophage anti-metastatic activity through IFN-gamma-STAT1 signaling, offering a therapeutic strategy for metastasis.

The paper analyzes rDNA copy number variation in humans, finding distinct associations with metabolic diseases and growth traits.

The paper identifies rRNA sequence variants affecting human traits and diseases by analyzing UK Biobank data and developing the RiboVAn method.

This study uses heterochronic myeloid cell replacement to show that the local brain environment, not intrinsic factors, drives microglia aging.

This paper creates a single-cell atlas of aging in C. elegans, revealing cell-type specific aging patterns and identifying transcription factors that regulate aging rates.

The paper analyzes replicative senescence in WI-38 cells using multi-omics data, finding early senescence markers, myofibroblast-like transitions, and YAP1/TEAD1 regulation.

The paper investigates age-related changes in muscle progenitors by analyzing single-cell RNA-seq data from young and aged mice, finding that differentiation amplifies age-related changes in progenitors but masks some changes.

The paper introduces a method to infer genome-wide regulatory causality using time-resolved gene expression data from yeast and validates its predictions experimentally.

This study uses single-cell RNA-seq to analyze aging in mice, finding that cell identity has a greater influence on aging trajectories than tissue environment.

Solo identifies doublets in scRNA-seq data using semi-supervised deep learning, improving accuracy over existing methods.

The paper introduces a new platform to study aging yeast by purifying old cells and analyzing their transcriptional and chromatin changes.