Chemotherapy, a primary treatment for cancer, can impair wound healing by affecting skin cells, macrophages, and other cells involved in the healing process. Chemotherapy drugs inhibit cellular metabolism, cell division, and angiogenesis, leading to delayed wound healing, chronic wounds, and skin complications such as rashes, folliculitis, hand-foot syndrome, and nerve damage. These effects are exacerbated when chemotherapy is combined with surgical tumor excision. The mechanisms involve interference with growth factors, cell migration, and extracellular matrix production, as well as disruption of immune responses and nerve function. Chemotherapy-induced peripheral neuropathy is a significant complication, affecting sensory nerves and impairing wound healing. It is associated with high doses, multiple treatment cycles, and certain chemotherapy agents. The effects of chemotherapy on the immune system, including reduced numbers of T cells, natural killer cells, and dendritic cells, also hinder wound healing by delaying the removal of dead tissue and increasing infection risk. Epigenetic changes caused by chemotherapy may contribute to impaired wound healing, although this area is not well studied. Epigenetic interventions, such as DNA methyltransferase inhibitors, show potential in promoting skin healing. Cell therapies, like autologous keratinocyte transplantation, are promising treatments for chemotherapy-induced wound healing issues. Adipose-derived mesenchymal stromal cells also show potential for wound healing. Despite the severity of chemotherapy-related wound healing complications, there are currently no specific treatments to prevent or mitigate these side effects. However, cell-based therapies and epigenetic interventions are emerging as potential solutions. The impact of chemotherapy on wound healing is an underexplored area that requires further research to improve patient outcomes and quality of life.Chemotherapy, a primary treatment for cancer, can impair wound healing by affecting skin cells, macrophages, and other cells involved in the healing process. Chemotherapy drugs inhibit cellular metabolism, cell division, and angiogenesis, leading to delayed wound healing, chronic wounds, and skin complications such as rashes, folliculitis, hand-foot syndrome, and nerve damage. These effects are exacerbated when chemotherapy is combined with surgical tumor excision. The mechanisms involve interference with growth factors, cell migration, and extracellular matrix production, as well as disruption of immune responses and nerve function. Chemotherapy-induced peripheral neuropathy is a significant complication, affecting sensory nerves and impairing wound healing. It is associated with high doses, multiple treatment cycles, and certain chemotherapy agents. The effects of chemotherapy on the immune system, including reduced numbers of T cells, natural killer cells, and dendritic cells, also hinder wound healing by delaying the removal of dead tissue and increasing infection risk. Epigenetic changes caused by chemotherapy may contribute to impaired wound healing, although this area is not well studied. Epigenetic interventions, such as DNA methyltransferase inhibitors, show potential in promoting skin healing. Cell therapies, like autologous keratinocyte transplantation, are promising treatments for chemotherapy-induced wound healing issues. Adipose-derived mesenchymal stromal cells also show potential for wound healing. Despite the severity of chemotherapy-related wound healing complications, there are currently no specific treatments to prevent or mitigate these side effects. However, cell-based therapies and epigenetic interventions are emerging as potential solutions. The impact of chemotherapy on wound healing is an underexplored area that requires further research to improve patient outcomes and quality of life.