Deciphering the Iron Metabolism and Ferroptosis in Diabetic Wound Healing

Abstract

Diabetic-related complications, such as delayed and incomplete wound healing, are an increasing concern in the realm of public health. Ferroptosis represents an innovative variant of cellular demise. Ferroptosis is currently thought to be an essential factor in the process of diabetic wound recovery. This article, therefore, examines the novel function and mechanism of ferroptosis in the repair of diabetic wounds. Diabetic hyperglycemia can induce a healing process that disrupts the function and activity of cells, thereby impeding the repair of diabetic wounds. Ferroptosis may be accelerated in diabetic lesions due to protracted low-level inflammation and oxidative stress induced by elevated glucose, according to the available evidence. As a result, the buildup of ferroptosis impedes cellular migration and proliferation, amplifies oxidative stress and the inflammatory response, and ultimately interferes with the wound-healing process. By regulating the expression of factors linked to iron mortality, this substance expedites wound healing and fosters angiogenesis in diabetic rodents. Moreover, new perspectives on the difficulties and outlooks related to ferroptosis in the context of diabetic wound healing are provided, thereby contributing to the progression of understanding in this field.