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The general case for redox control of wound repair
Author(s) -
Sen Chandan K.
Publication year - 2003
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1046/j.1524-475x.2003.11607.x
Subject(s) - reactive oxygen species , wound healing , redox , microbiology and biotechnology , oxygen , regeneration (biology) , growth factor , chemistry , biology , biochemistry , immunology , receptor , organic chemistry
The orthodox view has been that reactive oxygen species are primarily damaging to cells. There is general agreement that while high (3%) doses of H 2 O 2 may serve as a clinical disinfectant, its overall effect on healing is not positive. Current work shows that at very low concentrations, reactive oxygen species may regulate cellular signaling pathways by redox‐dependent mechanisms. Recent discoveries show that almost all cells of the wound microenvironment contain specialized enzymes that utilize O 2 to generate reactive oxygen species. Numerous aspects of wound healing are subject to redox control. An understanding of how endogenous reactive oxygen species are generated in wound‐related cells may influence the healing process and could result in new redox‐based therapeutic strategies. Current results with growth factor therapy of wounds have not met clinical expectations. Many of these growth factors, such as platelet‐derived growth factor, rely on reactive oxygen species for functioning. Redox‐based strategies may serve as effective adjuncts to jump‐start healing of chronic wounds. The understanding of wound‐site redox biology is also likely to provide novel insights into the fundamental mechanisms that would help to optimize conditions for oxygen therapy. While a window of therapeutic opportunity seems to exist under conditions of low concentrations of reactive oxygen species, high levels may complicate regeneration and remodeling of nascent tissue. (WOUND REP REG 2003;11:431–438)