Oxidative stress in normal and impaired wound repair.
A large percentage of the population suffers from wound healing abnormalities, in particular aged individuals, patients with diabetes, and those treated with immunosuppressive drugs, chemo- or radiotherapy. The mechanisms underlying the impaired healing response are still poorly understood. Recent studies provided strong evidence for a role of oxidative stress in the pathogenesis of non-healing ulcers. Therefore, it is of major importance to identify and functionally characterize the factors involved in the generation and detoxification of reactive oxygen species (ROS). This will provide the basis for the development of new strategies for therapeutic intervention. In this review we summarize the current information about the roles of low molecular weight antioxidants and ROS-detoxifying enzymes in normal and impaired wound repair, and we report on the consequences of their modulation at the wound site.
Schäfer
Matthias
M
ETH Zurich, Institute of Cell Biology, Schafmattstr. 18, HPM D42, CH-8093 Zürich, Switzerland.
Werner
Sabine
S
D000818:Animals; D000975:Antioxidants / Q000502:physiology; D002374:Catalase / Q000502:physiology; D005979:Glutathione Peroxidase / Q000502:physiology; D051547:Heme Oxygenase-1 / Q000502:physiology; D006801:Humans; D018384:Oxidative Stress / Q000502:physiology*; D054464:Peroxiredoxins / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D012867:Skin / Q000378:metabolism; D013482:Superoxide Dismutase / Q000502:physiology; D014945:Wound Healing / Q000502:physiology*
D000975:Antioxidants; D017382:Reactive Oxygen Species; D054464:Peroxiredoxins; D002374:Catalase; D005979:Glutathione Peroxidase; D051547:Heme Oxygenase-1; D013482:Superoxide Dismutase