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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

Wnt/モ-catenin signaling activator restores hair regeneration suppressed by diabetes mellitus
Yeong Chan Ryu 1 (Graduate student), You-rin Kim1 (Graduate student), Jiyeon Park1 (Graduate student), Sehee Choi1 (Graduate student), Geon-Uk Kim1 (Graduate student), Eunhwan Kim1 (Graduate student), Yumi Hwang1 (Graduate student), Heejene Kim1 (Graduate student), Soon Sun Bak3 (Research worker), Young Kwan Sung3 (Professor), Gyoonhee Han1 (Professor), Soung-Hoon Lee2 (Research worker), Kang-Yell Choi2,* (Professor)
1Biotechnology, Yonsei University,
2CK Regeon Inc,
3Immunology, Kyungpook National University
Diabetes mellitus is one of the most prevalent diseases in modern society. Many complications, such as hepatic cirrhosis, neuropathy, cardiac infarction, etc., are associated with diabetes. Although a relationship between diabetes and hair loss has been recently reported, the treatment of diabetic hair loss by Wnt/モ-catenin activators has not yet been achieved. In this study, we found that the depilation-induced anagen phase was delayed in both db/db, 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 the suppression of Wnt/モ-catenin signaling and decreased proliferation of hair follicle cells. We identified that KY19382, a small molecule that activates Wnt/モ-catenin signaling, restored the capabilities of regrowth and WIHN in diabetic mice. The Wnt/モ-catenin signaling activator also increased the length of the human hair follicle which was decreased under high glucose culture conditions. Overall, the diabetic condition reduces both hair regrowth and regeneration with suppression of the Wnt/モ-catenin signaling pathway. Consequently, the usage of Wnt/モ-catenin signaling activators could be a potential strategy for the treatment of diabetes-induced alopecia patients.
Abstract, Accepted Manuscript(in press) [Submitted on May 6, 2022, Accepted on August 2, 2022]
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