Wnt/β-catenin signaling activator restores hair regeneration suppressed by diabetes mellitus

Yeong Chan Ryu, You rin Kim, Jiyeon Park, Sehee Choi, Geon Uk Kim, Eunhwan Kim, Yumi Hwang, Heejene Kim, Soon Sun Bak, Jin Eun Lee, Young Kwan Sung, Gyoonhee Han, Soung Hoon Lee, Kang Yell Choi

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)


Diabetes mellitus is one of the most prevalent diseases in modern society. Many complicationssuch as hepatic cirrhosis, neuropathy, cardiac infarction, and so on are associated with diabetes. Although a relationship between diabetes and hair loss has been recently reported, the treatment of diabetic hair loss by Wnt/β-catenin activators has not been achieved yet. In this study, we found that the depilation-induced anagen phase was delayed in both db/db mice and high-fat diet (HFD) and streptozotocin (STZ)-induced diabetic mice. In diabetic mice, both hair regrowth and wound-induced hair follicle neogenesis (WIHN) were reduced because of suppression of Wnt/β-catenin signaling and decreased proliferation of hair follicle cells. We identified that KY19382, a small molecule that activates Wnt/β-catenin signaling, restored the capabilities of regrowth and WIHN in diabetic mice. The Wnt/β-catenin signaling activator also increased the length of the human hair follicle which was decreased under high glucose culture conditions. Overall, the diabetic condition reduced both hair regrowth and regeneration with suppression of the Wnt/β-catenin signaling pathway. Consequently, the usage of Wnt/β-catenin signaling activators could be a potential strategy to treat diabetes-induced alopecia patients.

Original languageEnglish
Pages (from-to)559-564
Number of pages6
JournalBMB reports
Issue number11
Publication statusPublished - 2022

Bibliographical note

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© This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology


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