Jessica L. Pierce

TL;DR: The data show that increasing kyn levels results in accelerated skeletal aging by impairing osteoblastic differentiation and increasing osteoclastic resorption, and suggest that kyn could play a role in age‐induced bone loss.

TL;DR: Establishing a better understanding of fat storage in bone marrow cells, as well as the osteoblast-adipocyte relationship within the bone marrow niche is necessary to understand the mechanisms underlying disease- and aging-related marrow fat storage and may lead to the development of new therapeutic targets for "fatty bone" and osteoporosis.

TL;DR: Surprisingly, despite decreasing senescent cell burden, navitoclax treatment decreased trabecular bone volume fraction in aged female and male mice, and BMSC-derived osteoblasts from the navitClax treated mice were impaired in their ability to produce a mineralized matrix, suggesting a potentially harmful effect of navitclax on skeletal-lineage cells.

TL;DR: Reduced Hdac3 activity in osteochondroprogenitor cells contributes to increased marrow adiposity associated with aging, and concurrent declines in transcription and phosphorylation combine to suppress HdAC3Activity in aging bone.

TL;DR: Novel molecular pathways involved in KYN's age-associated effects in the bone microenvironment that may be useful translational targets for treating osteoporosis are revealed.