Adipocyte Kindlin-2 Coordinates an E-cadherin/β-catenin/IGFBP2 Endocrine Axis to Regulate Skin Regeneration and Diabetic Wound Healing

Adipocyte-specific Kindlin-2 loss in mice markedly accelerates skin wound closure by boosting fibroblast proliferation, angiogenesis, and suppressing inflammation.

• Why it matters: Adipose tissue’s endocrine control of cutaneous regeneration is not well defined, limiting targeted therapies for chronic and diabetic wounds.
• What they did: The study used adipocyte-specific Kindlin-2 deletion and vWAT transplantation in mice, then mapped a pathway where E-cadherin proteolysis releases a 33-kDa CTF2 that activates {beta}-catenin signaling to induce IGFBP2.
• The result: Blocking {beta}-catenin signaling removed the healing benefit, while lentiviral IGFBP2 delivery significantly accelerated wound closure in wild-type C57BL/6 and diabetic ob/ob mice.

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