AI Article Synopsis

  • - Recessive dystrophic epidermolysis (RDEB) is a genetic skin disorder that causes painful blisters and chronic wounds, with no current cure available.
  • - A clinical trial treated 14 RDEB patients with three infusions of ABCB5 mesenchymal stromal cells (MSCs), leading to improved healing of existing wounds and a decrease in the formation of new wounds.
  • - A detailed analysis indicated that the newly formed wounds healed more quickly and stayed closed longer, suggesting that ABCB5 MSCs may help stabilize the skin and could benefit RDEB treatment with ongoing therapy.

Article Abstract

Recessive dystrophic epidermolysis (RDEB) is a rare, inherited, and currently incurable skin blistering disorder characterized by cyclically recurring wounds coexisting with chronic non-healing wounds. In a recent clinical trial, three intravenous infusions of skin-derived ABCB5 mesenchymal stromal cells (MSCs) to 14 patients with RDEB improved the healing of wounds that were present at baseline. Since in RDEB even minor mechanical forces perpetually provoke the development of new or recurrent wounds, a post-hoc analysis of patient photographs was performed to specifically assess the effects of ABCB5 MSCs on new or recurrent wounds by evaluating 174 wounds that occurred after baseline. During 12 weeks of systemic treatment with ABCB5 MSCs, the number of newly occurring wounds declined. When compared to the previously reported healing responses of the wounds present at baseline, the newly occurring wounds healed faster, and a greater portion of healed wounds remained stably closed. These data suggest a previously undescribed skin-stabilizing effect of treatment with ABCB5 MSCs and support repeated dosing of ABCB5 MSCs in RDEB to continuously slow the wound development and accelerate the healing of new or recurrent wounds before they become infected or progress to a chronic, difficult-to-heal stage.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10252830PMC
http://dx.doi.org/10.3390/cells12111468DOI Listing

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