Fibro-inflammatory progenitors represent a subpopulation of perivascular cells in visceral adipose tissues of mice that promote inflammation and fibrosis.

Bioinformatic analysis of mesenchymal stem cell chondrogenesis identified a novel long noncoding RNA, GRASLND, which suppresses interferon signaling and enhances chondrogenesis.

A group of cells that can become adipocytes controls the formation of blood vessels in the bone marrow, and also regulates the differentiation of resident mesenchymal progenitor cells.

A newly identified adipose lineage cell population, MALP, regulates marrow vasculature and osteogenesis in bone.

Estrogen aggravates mammary involution through lysosome-mediated cell death, neutrophil recruitment via CXCR2 signalling, neutrophil-mediated inflammation and adipocyte repopulation.

Murine periosteum is highly enriched for osteoprogenitors, many of which express αSMA, but fracture callus chondrocytes are partially derived from other sources.

Adipsin, the oldest known adipokine, has a novel role as a a regulator of bone marrow fat and, consequently, overall bone health.

A novel secondary adipogenesis pathway is defined that is unique to the bone marrow and is activated with age and in states of metabolic stress.

Hypertrophic chondrocytes of the growth plate undergo a process of dedifferentiation to generate marrow associated skeletal stem and progenitor cells (SSPCs), which ultimately re-differentiate into cells of the osteoblast or adipocyte lineages during skeletal development.

A novel population of adipocytes that play essential roles in adaptive thermogenesis via cell autonomous and non-autonomous effects and regulate systemic glucose metabolism in mice.