Nerve is the foundation of the physiological function such as the skin feeling and thermoregulation, and also regulates the regeneration and scar healing of skin wound by multiple mechanisms. Though the denervated skin wound can heal spontaneously, the nerve might accelerate wound healing by activating the neurogenic inflammation and nerve trophism, increasing the blood supply around the wound, promoting the proliferation of fibroblasts and keratinocytes, stimulating the expression of collagen I and III, and interacting with immune system and releasing neuropeptides. If all kinds of repair cells, extracellular matrix, nerve, blood vessel and cutaneous appendages assemble organically, the skin wound regenerates, and otherwise the scar heals. The nerve axon growth occurs mainly in the early stage of the wound healing and the scar rebuilding process, and the nerve growth rate is obviously slower than the granulation tissue formation and cicatrization. Furthermore, the axon growth of different nerve fibers are not entirely the same. The exogenous neuropeptides might promote the wound repair and the nerve regeneration. The antagonist of the neuropeptides or high selective nerve abscission might reduce the scar hyperplasia. Therefore, it contribute to find methods to promote the regeneration of skin wound and peripheral nerve injury by understanding the effects and regulatory mechanism of both nerve and various repair elements in regeneration or scar healing of skin wound.

Ex vivo culture-amplified mesenchymal stem cells (MSCs) have been studied because of their capacity for healing tissue injury. MSC transplantation is a valid approach for promoting the repair of damaged tissues and replacement of lost cells or to safeguard surviving cells, but currently the efficiency of MSC transplantation is constrained by the extensive loss of MSCs during the short post-transplantation period. Hence, strategies to increase the efficacy of MSC treatment are urgently needed. Iron overload, reactive oxygen species deposition, and decreased antioxidant capacity suppress the proliferation and regeneration of MSCs, thereby hastening cell death. Notably, oxidative stress (OS) and deficient antioxidant defense induced by iron overload can result in ferroptosis. Ferroptosis may inhibit cell survival after MSC transplantation, thereby reducing clinical efficacy. In this review, we explore the role of ferroptosis in MSC performance. Given that little research has focused on ferroptosis in transplanted MSCs, further study is urgently needed to enhance the in vivo implantation, function, and duration of MSCs.
Humans ; Antioxidants/metabolism* ; Ferroptosis ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stem Cells ; Iron Overload/metabolism*