Figure 3. Signalling crosstalk between dWAT and hair follicles in mice.

(a) During early, refractory telogen, dermal adipocytes signal to inhibit anagen entry by hair follicles. This inhibitory effect is in part mediated by dermal adipocyte-derived Bmp ligands²⁸. (b) During late, competent telogen, dermal adipocytes reduce Bmp ligand production. Reduction in hair cycle inhibitors enables hair follicles to easily respond to other growth-activating stimuli; hence they become competent^11,26,28. At the same time, adipose progenitors secrete Pdgfα, which has hair cycle-activating effects⁶. (c) During anagen, enlarged hair follicles secrete ligands for multiple pro-adipogenic signalling pathways, including Bmp⁴⁸ and Hedgehog⁴⁵. These ligands act on dermal preadipocytes to stimulate their differentiation into lipid-laden adipocytes. Other putative signals from hair follicles, not indicated here, could also induce adipogenesis. (d) During catagen, dWAT reduces in size, mediated, in part, by lipolysis. The signalling mechanism of dWAT reduction is not fully understood, but it probably involves the loss of HF-derived adipogenic activators and/or production of additional anti-adipogenic factors.