Interesting. At least during natural hair cycling, FGF-5 has been proposed to induce catagen with some real-world support for this assumption [1]. The original study [2] for this patent, however, only found that people with abnormally long hair (megatrichology) through FGF-5 mutation cease to have this condition when FGF-5 is fixed. In their case, too long hair was probably caused through a much extended anagen phase. In the case of Androgenetic Alopecia, we suffer from very short anagen and too long catagen.
Question is: Does FGF-5 only regulate the temporal length of catagen directly, or is it a "side" effect of FGF-5 actually modulating DP/DSC cell apoptosis? If it's the former, it is of no use of us. In the latter case, however, it would be a viable approach.
[1] "An Investigation of Apoptosis in Androgenetic Alopecia", Michael B. Morgan and Paul Rose, Annals of Clinical & Laboratory Science, vol. 33, no. 1, 2003,
http://www.annclinlabsci.org/content/33/1/107.full.pdf
[2] "FGF5 is a crucial regulator of hair length in humans", Higgins et al., Proceedings of the National Academy of Sciences,
http://www.ncbi.nlm.nih.gov/pubmed/24989505
