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GCDFP-15 impairs diabetic cutaneous wound repair in mice by suppressing the PI3K-AKT-mTOR-STAT3 pathway

Chengmei Zhang1,2, Qian Wan1,2, Hua Zhou1,2

  • 1The First People's Hospital of Chenzhou Affliated to the University of South China, Chenzhou, Hunan, China.

Archives of Physiology and Biochemistry
|April 20, 2026
PubMed

Insights

Prolactin-induced protein (GCDFP-15) hinders diabetic wound healing by suppressing pro-reparative signals. Blocking GCDFP-15 enhances healing, angiogenesis, and macrophage function in diabetic wound models.

Area of Science:

  • Biomedical Science
  • Wound Healing Research
  • Immunology

Background:

  • Diabetic wound healing is impaired by poor angiogenesis and immune dysfunction.
  • Prolactin-induced protein (GCDFP-15) is upregulated in diabetic wound transcriptomes.
  • GCDFP-15's role in wound repair was previously unknown.

Purpose of the Study:

  • To investigate the functional role of GCDFP-15 in diabetic wound healing.
  • To determine GCDFP-15's impact on angiogenesis and immune cell phenotypes.
  • To elucidate the molecular pathways regulated by GCDFP-15.

Main Methods:

  • Utilized murine diabetic wound models.
  • Employed genetic deletion (knockout) of GCDFP-15.
  • Administered topical recombinant GCDFP-15 protein.

Main Results:

  • GCDFP-15 genetic deletion accelerated wound closure and enhanced angiogenesis.
  • Deletion of GCDFP-15 promoted a pro-reparative macrophage phenotype.
  • Topical GCDFP-15 impaired healing and inhibited the PI3K/AKT/mTOR/STAT3 pathway.
  • GCDFP-15 deletion activated the PI3K/AKT/mTOR/STAT3 signalling axis.

Conclusions:

  • GCDFP-15 acts as an endogenous inhibitor of diabetic wound repair.
  • GCDFP-15 suppresses pro-reparative signalling pathways.
  • Targeting GCDFP-15 presents a potential therapeutic strategy for diabetic wounds.
Keywords:
GCDFP-15PI3K-AKT-mTORangiogenesisdiabetic wound healingmacrophage polarisation

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