Dermal white adipose tissue renewal is regulated by the PDGFA/AKT axis
Disesteemed for many years as tissue exclusively dedicated to energy storage, the white adipose tissue (WAT) has become one of the most studied tissues, especially as recent reports uncovered its metabolic and endocrine functions in vivo contributing to the development of metabolic disorders, control of immune response and wound healing processes. The traditional classification of WAT describes two distinct anatomical depots, namely subcutaneous WAT (sWAT) and visceral WAT (vWAT), which exhibit differences at the cellular level and in structure (1). These differences may also be responsible for depot-specific WAT function and affect tissue plasticity and remodeling. More recently, a third type of WAT, which is referred to as dermal WAT (dWAT), received high appreciation, as it was identified as central contributor in skin-relevant processes including hair follicle growth, thermoregulation and wound healing (1). In contrast to long-lived adipocytes in sWAT and vWAT-depots, dWAT is characterized by rapid adipocyte turnover, adipocyte-myofibroblast plasticity and depot-specific cytokine profiles that have an impact on the differentiation and self-renewal abilities of skin regenerative cells, especially hair follicle stem cells. Due to these specificities, self-renewal of adipocyte progenitor cells and regulation of tissue homeostasis in dWAT is suggested to be differentially regulated compared to the other WAT depots. To address this issue Rivera-Gonzales et al. (2) established a mouse model to investigate the molecular mechanisms specifically regulating tissue homeostasis in dWAT.