12 citations
,
August 2020 in “Frontiers in Genetics” This study suggests that the long noncoding RNA H19 helps dermal papilla cells maintain their hair follicle-inducing ability by activating the Wnt signaling pathway, potentially offering a therapeutic target for androgenetic alopecia.
54 citations
,
April 2019 in “Journal of cellular physiology” In this study, miR-218-5p was found to enhance hair shaft growth and positively regulate the Wnt signaling pathway by targeting SFRP2 during skin and hair follicle development.
23 citations
,
August 2017 in “Genome” This study identified several genes and signaling pathways, such as Wnt and MAPK, involved in fur development in Chinchilla rex rabbits, providing insights into skin and hair follicle growth.
25 citations
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January 2014 in “Annals of Dermatology” Sfrp2 increases during hair follicle catagen phase and slows keratinocyte growth.
170 citations
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July 2012 in “Journal of Investigative Dermatology” In this study, researchers showed that Wnt ligands secreted by hair follicle epithelium are crucial for hair follicle regeneration and may be significant for treating hair disorders like alopecia.
40 citations
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June 2011 in “Journal of biological chemistry/The Journal of biological chemistry” This study revealed that deficiency in the enzyme FA2H in mice affected sebaceous gland function, altered sebum composition, and caused cycling alopecia, highlighting FA2H's role in hair follicle homeostasis.
224 citations
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March 2006 in “Seminars in Cutaneous Medicine and Surgery” This article discusses the hair follicle's regenerative cycles and the molecular mechanisms influencing them, emphasizing the need for therapeutic targeting of the "hair cycle clock" to manage hair growth disorders, without reporting new research findings.
71 citations
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February 2000 in “Endocrinology and metabolism/American journal of physiology: endocrinology and metabolism” This study found that topical estradiol inhibits hair growth in mice by preventing the hair follicle's transition from resting to growth phase, a process reversible with an estrogen receptor antagonist.