Fig. 1

Signaling molecules involved in the hair cycle. (a) In telogen, bone morphogenetic proteins (BMPs), such as BMP4 from endothelial cells, BMP2 from adipocytes, and BMP4 from fibroblasts, maintain the quiescence of hair follicle stem cells (HFSCs). Oncostatin M (OSM) released by TREM2⁺ macrophages, and fibroblast growth factor 18 (FGF18) from the dermal papilla (DP) and bulge, also contribute to the dormancy of HFSCs. (b) During the transition from telogen to anagen, factors like FGF7, FGF10, Norrin, and BMP inhibitors (Noggin and transforming growth factor-β2 (TGFβ2)) promote the activation of HFSCs. Other contributors to this shift include endothelin 1 (EDN1) from endothelial cells, platelet-derived growth factor subunit A (PDGFA) from adipocyte precursor cells, and Wnts (Wnt7b and Wnt10a) from apoptotic CD11b⁺ macrophages. Additionally, cutaneous transient receptor potential cation channel subfamily V member 1 (TRPV1) innervations accelerate hair growth via Spp1 from CD9⁺CD26⁺ fibroblasts. (c) In anagen, sonic hedgehog (SHH) from transit-amplifying cells (TACs) further enhances the proliferation of HFSCs and the differentiation of adipocyte precursor cells, leading to the extension of hair follicles. (d) During the anagen-catagen transition, FGF5 from the matrix and outer root sheath (ORS), and Wnt antagonists (dickkopf WNT signaling pathway inhibitor 2 (DDK2) and Notum) from the DP induce the apoptosis of follicular cells. (e) In catagen, epithelial cells release EDN1 to stimulate calcium influx and dermal sheath retraction to relocate the DP. (f) In the subsequent telogen, the DP and the new bulge are positioned adjacent to the old bulge. Fig. 1 was adapted from [2] (Zhang B, Chen T. Local and systemic mechanisms that control the hair follicle stem cell niche. Nat Rev Mol Cell Biol. 2024;25(2):87-100. https://www.nature.com/nrm/), which is not part of the governing OA license, with reproduction permission.