CD107a expression divides osteogenic from adipogenic perivascular precursor cells within human white adipose tissue.

The size of subcutaneous, but not visceral, fat depots is dependent on the number of embryonic adipocyte progenitors.

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

Combined fate mapping and genetic deletion studies reveal that PDGFRα+ cells and PDGFRα gene itself are required for adipose tissue development but not for adult tissue homeostasis.

A hybrid mouse/human model using mesenchymal progenitor cells reveals dynamics of human adipose tissue development and mechanisms that may enhance human adipose thermogenic capacity.

Single-cell expression profiling and genetic lineage analysis show that aging impairs adipocyte differentiation from precursor cells and blocks the thermogenic activation of adipocytes during cold exposure.

Identification of bone marrow Adipoq-lineage progenitors as a novel and major cellular source of M-CSF in mice and humans, which controls bone marrow macrophage development, osteoclastogenesis, and bone mass in physiological and pathological conditions.

Adipose tissue derived hematopoietic stem cells from diabetic mice transplanted into healthy animals on a normal diet increase inflammation in adipose tissue and trigger the development of a diabetic state in the recipient animals.

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

Diet-induced obesity in mice led to a duration of diet-dependent bone marrow adipocyte whitening, which drove monocyte expansion and skewing towards a tissue-invasive phenotype, likely contributing to ensuing tissue infiltration that accompanies obesity and diabetes.