David G. Monroe

The paper examines p21Cip1 and p16Ink4a expression in senescent cells across tissues, revealing heterogeneity and tissue-specific SASP profiles.

This study presents a longitudinal assessment of age-related changes in Brown-Norway rat physiology and histopathology at 6, 17, and 27 months of age to provide healthspan parameters for aging research.

This study identifies p21+ senescent-like cells, including osteochondroprogenitors and neutrophils, as key regulators of fracture repair, showing their distinct roles from age-related p16+ senescent cells.

This study shows that cellular senescence drives bone marrow adiposity in radiation- and aging-associated bone loss through miR-27a upregulation and senolytic treatment reduces BMAT.