Perivascular extracellular vesicles induce bone repair, and do so via tetraspanin binding to recipient skeletal progenitor cells.

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

Aging is associated with stress-induced senescence of adipose stromal cells, leading to impaired adipogenesis, oxidative stress, mitochondrial dysfunction, and insulin resistance, all being alleviated by metformin treatment of adipose stromal cells.

A rigorous and transparent evaluation of mesenchymal stem cell therapy for sepsis suggests it may be efficacious, although the strength of these findings is tempered by threats to validity in the studies that were included.

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

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

Senescent cells contribute to age-related fat dysfunction and can directly impair healthy fat progenitor function, in part, via the secretion of activin A.

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.

Disruption of epoxide hydrolysis inducing oxidative stress and cellular senescence is a novel mechanism responsible for lipoatrophic monogenic diabetes.

Protein kinase A (PKA) phosphorylates Raptor and inhibits mammalian target of rapamycin complex 1 (mTORC1) activity.