MiR-221-3p facilitates cutaneous wound healing in diabetic mice.

The persistent non-healing of cutaneous wounds in diabetic patients represents a critical clinical challenge requiring urgent resolution. Excessive inflammation, impaired angiogenesis, and aberrant collagen remodeling profoundly hinder wound recovery. This study explores the potential therapeutic value of miR-221-3p in diabetic cutaneous wound healing using murine models. Subcutaneous administration of miR-221-3p was associated with accelerated wound closure; histological staining and Western blot analyses showed decreased expression of inflammatory markers (IL-1β, IL-6, MPO, CD68), increased levels of angiogenic markers (CD31, VEGFA), and enhanced collagen I/III deposition at wound margins. Complementary experiments using Mir221 knockout mice showed delayed healing, which was accompanied by upregulated MPO/CD68 expression, reduced CD31 levels, and decreased collagen fiber formation. These bidirectional observations suggest that miR-221-3p may contribute to diabetic wound healing, potentially through effects on inflammatory responses, neovascularization, and collagen synthesis. These findings suggest that miR-221-3p could serve as a potential therapeutic target for refractory wounds in diabetic patients, including diabetic foot ulcers and other chronic cutaneous lesions.