142 citations
,
February 2016 in “Science” 56 citations
,
September 2014 in “Molecular Endocrinology”
25 citations
,
August 2014 in “Endocrinology” Researchers created a mouse model of a type of rickets that does not cause hair loss.
426 citations
,
August 2014 in “Nature Medicine” Skin stem cells interacting with their environment is crucial for maintaining and regenerating skin and hair, and understanding this can help develop new treatments for skin and hair disorders.
21 citations
,
March 2014 in “Clinical and experimental dermatology” Targeting the Wnt pathway might help treat hair loss.
107 citations
,
March 2014 in “BoneKEy Reports” Mutations in the vitamin D receptor cause hereditary vitamin D-resistant rickets, leading to poor bone health and requiring high calcium doses for treatment.
218 citations
,
October 2013 in “Proceedings of the National Academy of Sciences of the United States of America” Mice lacking the PPARγ gene in their fat cells had almost no fat tissue, severe metabolic problems, and abnormal development of other fat-related tissues.
499 citations
,
September 2011 in “Cell” Fat-related cells are important for initiating hair growth.
37 citations
,
April 2011 in “Journal of Biological Chemistry” LEF1 interacts with Vitamin D Receptor, affecting hair follicle regeneration and this could be linked to hair loss conditions.
53 citations
,
May 2010 in “Journal of Cellular Physiology” Mice without Vitamin D receptors have hair growth problems because of issues in the hedgehog signaling pathway.
127 citations
,
January 2008 in “PloS one” Vitamin D receptor helps control hair growth and could be used to treat certain skin tumors.
143 citations
,
May 2007 in “Proceedings of the National Academy of Sciences” Vitamin D receptor is crucial for normal hair growth and preventing hair loss.
95 citations
,
July 2006 in “British Journal of Dermatology”
375 citations
,
February 2006 in “Journal of Cell Science” The document concludes that the hair cycle is a complex process involving growth, regression, and rest phases, regulated by various molecular signals.
144 citations
,
December 2004 in “Molecular Endocrinology” 297 citations
,
January 2002 in “Development” The study investigated the effects of repressing β-catenin/Lef1 signalling in mouse epidermis by expressing a ΔNLef1 transgene. Mice showed no skin abnormalities before the first postnatal hair cycle, but from 6 weeks of age, they experienced progressive hair loss and developed dermal cysts originating from hair follicles. These cysts expressed markers of interfollicular epidermis. Adult mice spontaneously developed skin tumours, mostly with sebaceous differentiation, suggesting an origin in the upper hair follicle. The transgene was expressed in the tumours, inhibiting β-catenin signalling, as shown by the absence of cyclin D1 expression, while patched mRNA was upregulated, implicating the sonic hedgehog pathway in tumour formation. The study concluded that β-catenin signalling levels determine keratinocyte differentiation into hair or interfollicular epidermis, and that ΔNLef1 overexpression can lead to skin tumours.
115 citations
,
December 2001 in “Endocrinology” 137 citations
,
April 2001 in “Journal of Clinical Investigation” 114 citations
,
June 2000 in “Endocrinology” 29 citations
,
June 2000 in “Endocrinology” 519 citations
,
October 1998 in “Endocrinology” Diet can prevent bone issues but not hair loss in mice lacking vitamin D receptors.