Table 1.

The markers of hair follicle and their role.

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

HF: hair follicle; HS: hair shaft; DP: dermal papilla; SC: stem cell.