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PDZ-RhoGEF controls adipose tissue abundance and whole body metabolism.

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 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.

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

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

A brown-to-white adipogenic transdifferentiation process in the periureter region of mouse renal adipose tissue gives rise to a population of cold-inducible adipocytes with a transcriptome distinct from subcutaneous beige adipocytes.

Significant technical improvement in single-nucleus RNA-seq reveals distinct adipocyte subpopulations that respond differently to obesity, including those undergoing adaptive healthy expansion and others displaying severe dysfunction.

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

Normal adipogenesis requires de novo DNA methyltransferase 3A (DNMT3A) for proper differentiation and suppression of an age-associated pathogenic inflammatory program.

Single-cell RNA-sequencing, spatial genomics, and histological analyses reveal that cold-induced brown adipose neogenesis is a complex adaptive response to elevated metabolic demand involving dynamic interactions between recruited immune cells and a subpopulation of poised adipocyte progenitors.