Liraglutide Promotes Diabetic Wound Healing via Myo1c/Dock5

Abstract: Non‐healing diabetic wounds and ulcer complications, with persistent cell dysfunction and obstructed cellular processes, are leading causes of disability and death in patients with diabetes. Currently, there is a lack of guideline‐recommended hypoglycemic drugs in clinical practice, likely due to limited research and unclear mechanisms. In this study, it is demonstrated that liraglutide significantly accelerates wound closure in diabetic mouse models (db/db mice and streptozotocin‐induced mice) by improving re‐epithelialization, collagen deposition, and extracellular matrix remodeling, and enhancing the proliferation, migration, and adhesion functions of keratinocytes. However, these effects of improved healing by liraglutide are abrogated in dedicator of cytokinesis 5 (Dock5) keratinocyte‐specific knockout mice. Mechanistically, liraglutide induces cellular function through stabilization of unconventional myosin 1c (Myo1c). Liraglutide directly binds to Myo1c at arginine 93, enhancing the Myo1c/Dock5 interaction by targeting Dock5 promoter and thus promoting the proliferation, migration, and adhesion of keratinocytes. Therefore, this study provides insights into liraglutide biology and suggests it may be an effective treatment for diabetic patients with wound‐healing pathologies.

Location
Deutsche Nationalbibliothek Frankfurt am Main
Extent
Online-Ressource
Language
Englisch

Bibliographic citation
Liraglutide Promotes Diabetic Wound Healing via Myo1c/Dock5 ; day:19 ; month:08 ; year:2024 ; extent:13
Advanced science ; (19.08.2024) (gesamt 13)

Creator
Zhang, Qian
Zhang, Chunlin
Kang, Changjiang
Zhu, Jiaran
He, Qingshan
Li, Hongwei
Tong, Qiang
Wang, Min
Zhang, Linlin
Xiong, Xin
Wang, Yuren
Qu, Hua
Zheng, Hongting
Zheng, Yi

DOI
10.1002/advs.202405987
URN
urn:nbn:de:101:1-2408201430127.098538682499
Rights
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
Last update
24.03.2026, 10:40 AM CET

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Associated

  • Zhang, Qian
  • Zhang, Chunlin
  • Kang, Changjiang
  • Zhu, Jiaran
  • He, Qingshan
  • Li, Hongwei
  • Tong, Qiang
  • Wang, Min
  • Zhang, Linlin
  • Xiong, Xin
  • Wang, Yuren
  • Qu, Hua
  • Zheng, Hongting
  • Zheng, Yi

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