|
| Author | Signal | Researched object | Conclusions |
|
| Telerman et al., 2017 [91] | Blimp1 | Transgenic mouse | Ablation delayed HF morphogenesis, and growth and prevented new HF formation after wounding; role in promoting the dermal papilla inductive signaling cascade that initiates HF growth |
| Kobielak et al., 2007 [92] | Bmpr1a | Transgenic mouse | Ablation leads quiescent SCs to activate and to proliferate, causing an expansion of the niche and loss of slow-cycling cells; HFSCs are unable to terminally differentiate into hair |
| Lei et al., 2014 [93] | DKK1 | Transgenic mouse | DKK reduce hair follicle enlargement and decrease proliferation; injection of DKK1 during early anagen significantly reduced the width of prospective hairs |
| Millar et al., 1999 [94] | Dvl2 | Transgenic mouse | Overexpression in the outer root sheath causes the short-hair phenotype |
| Lin et al., 2015 [95] | FGF1, FGF2, FGF10 | Transgenic mouse | Topical application of FGFs induced an earlier anagen phase and prolonged the mature anagen phase; FGFs promoted hair growth by inducing the anagen phase in telogenic mice |
| Kimura-Ueki et al., 2012 [96] | FGF18 | Transgenic mouse | Ablation causes telogen to become very short, giving rise to a strikingly rapid succession of hair cycles |
| Higgins et al., 2014 [97] | FGF5 | DNA from families with long eyelashes | FGF5 is associated with long-hair phenotype |
| Guo et al., 1993 [98] | FGF7 | Transgenic mouse | Overexpression causes marked suppression of hair follicle morphogenesis |
| Petiot et al., 2003 [99] | Fgfr2 | Transgenic mouse | Lack of Fgfr2 leads to a decreased number of HFs, and follicles were developmentally retarded |
| Öztürk et al., 2015 [100] | Gab1 | Transgenic mouse | Lack of Gab1 caused HF not to enter catagen; instead HFSCs lose quiescence |
| Mill et al., 2003 [101] | Gli2 | Transgenic mouse | Lack of Gli2 causes arrest in HF development with reduced cell proliferation and Shh-responsive gene expression, but normal epidermal differentiation |
| Estrach et al., 2006 [102] | Jagged-1 | Transgenic mouse | Deletion of Jagged-1 results in inhibition of the hair growth cycle and conversion of hair follicles into cysts of cells undergoing interfollicular epidermal differentiation |
| Amalia Pasolli et al., 2014 [103] | LHX2 | Transgenic mouse | Ablation of LHX2 results in cellular disorganization and HFSC polarization within the niche. LHX2 loss leads to a failure to maintain HFSC quiescence and hair anchoring and progressive transformation of the niche into a sebaceous gland |
| Öztürk et al., 2015 [100] | Mapk | Transgenic mouse | Activation of Mapk signaling can restore quiescence of the SCs |
| Du et al., 2018 [104] | miR-214 | Human scalp skin tissue; in vitro | Downregulation of miR-214 promotes the proliferation and differentiation of HFSCs; overexpression of miR-214 led to decreased expression of EZH2, β-catenin, and TCF4 |
| Horsley et al., 2008 [105] | Nfatc1 | Transgenic mouse | Ablation causes stem cells to be activated prematurely, resulting in precocious follicular growth |
| Krieger et al., 2018 [106] | NF-κB | Transgenic mouse | Role in HF stem/progenitor cell activation during anagen induction, involvement in hair fiber morphogenesis during HF cycling |
| Demehri and Kopan, 2009 [107] | Notch | Transgenic mouse | Absence of Notch signaling leads bulge stem cell descendents to retain their capacity to execute the follicular differentiation program but failing to maintain it owing to their genetic deficiency |
| Lin et al., 2011 [108] | Pofut1 | Transgenic mouse | Disruption of Pofut1 in HF resulted in aberrant telogen morphology, a decrease of bulge SC markers; HF displayed a delay in anagen reentry and dysregulation of proliferation and apoptosis during the hair cycle transition |
| Oro and Higgins, 2003 [109] | Ptch | Transgenic mouse | Reduced Ptch is associated with tumor formation during anagen |
| Hoi et al., 2010 [110] | Runx1 | Transgenic mouse | Role in promoting anagen onset and HFSC proliferation |
| St- Jacques et al., 1998 [111] | Shh | Transgenic mouse | Shh signaling is not required for initiating hair follicle development; however, it is essential for controlling ingrowth and morphogenesis of the hair follicle |
| Kadaja et al., 2014 [112] | Sox9 | Transgenic mouse | Sox9-deficient bulge HFSCs begin to differentiate into epidermal cells; as HFSC numbers dwindle, outer root sheath production is not sustained, and HF down-growth arrests prematurely |
| Foitzik et al., 2000 [113] | TGF-β1 | Transgenic mouse | Injection of TGF-beta1 induced premature catagen development |
| Foitzik et al., 1999 [114] | TGF-β2 | Transgenic mouse | Ablation causes delay of hair follicle morphogenesis, with a 50% reduced number of hair follicles |
| Oshimori and Fuchs, 2012 [115] | TGF-βRII | Transgenic mouse | TGF-β2 signaling antagonizes BMP signaling in HFSCs with increased telogen length |
| Qiu et al., 2017 [116] | TPA | Transgenic mouse | Refractory telogen hair follicles entered anagen prematurely after TPA treatment, with the enhanced proliferation of CD34-positive hair follicle stem cells |
| Lei et al., 2014 [93] | Wnt10b | Transgenic mouse | Prolonged overexpression increased the size of regenerated hair follicles and increased expression of CD34 in the bulge |
| Millar et al., 1999 [94] | Wnt3 | Transgenic mouse | Overexpression causes a short-hair phenotype and cyclical balding resulting from hair shaft structural defects |
| Dong et al., 2017 [117] | Wnt7a | Transgenic mouse | Cultured human umbilical cord-MSCs (UC-MSCs) overexpressing Wnt7a can accelerate wound repair and induce hair regeneration via cellular communication in the wound microenvironment |
| Kandyba and Kobielak, 2013 [118] | Wnt7b | Transgenic mouse | Underexpression causes shorter anagen, premature catagen onset with overall shorter hair production, and diminished HF differentiation marker expression |
| Enshell-Seijffers et al., 2010 [119] | β-Catenin | Transgenic mouse | Inactivation in DP of HF results in reduced proliferation of the progenitors and their immediate progeny that generate the HS and premature catagen |
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