The general case for redox control of wound repair

被引:148
作者
Sen, CK [1 ]
机构
[1] Ohio State Univ, Med Ctr, Dorothy M Davis Heart & Lung Res Inst, Lab Mol Med,Dept Surg, Columbus, OH 43210 USA
关键词
D O I
10.1046/j.1524-475X.2003.11607.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The orthodox view has been that reactive oxygen species are primarily damaging to cells. There is general agreement that while high (3%) doses of H2O2 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 02 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.
引用
收藏
页码:431 / 438
页数:8
相关论文
共 98 条
[1]   Human neutrophil immunodeficiency syndrome is associated with an inhibitory Rac2 mutation [J].
Ambruso, DR ;
Knall, C ;
Abell, AN ;
Panepinto, J ;
Kurkchubasche, A ;
Thurman, G ;
Gonzalez-Aller, C ;
Hiester, A ;
deBoer, M ;
Harbeck, RJ ;
Oyer, R ;
Johnson, GL ;
Roos, D .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (09) :4654-4659
[2]   Reactive oxygen generated by Nox1 triggers the angiogenic switch [J].
Arbiser, JL ;
Petros, J ;
Klafter, R ;
Govindajaran, B ;
McLaughlin, ER ;
Brown, LF ;
Cohen, C ;
Moses, M ;
Kilroy, S ;
Arnold, RS ;
Lambeth, JD .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (02) :715-720
[3]   Hydrogen peroxide mediates the cell growth and transformation caused by the mitogenic oxidase Nox1 [J].
Arnold, RS ;
Shi, J ;
Murad, E ;
Whalen, AM ;
Sun, CQ ;
Polavarapu, R ;
Parthasarathy, S ;
Petros, JA ;
Lambeth, JD .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (10) :5550-5555
[4]   NADPH oxidase: An update [J].
Babior, BM .
BLOOD, 1999, 93 (05) :1464-1476
[5]   OXYGEN-DEPENDENT MICROBIAL KILLING BY PHAGOCYTES .1. [J].
BABIOR, BM .
NEW ENGLAND JOURNAL OF MEDICINE, 1978, 298 (12) :659-668
[6]   THE ENZYMATIC BASIS FOR (O-2).- PRODUCTION BY HUMAN-NEUTROPHILS [J].
BABIOR, BM .
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY, 1982, 60 (11) :1353-1358
[7]   Platelet-derived growth factor-induced H2O2 production requires the activation of phosphatidylinositol 3-kinase [J].
Bae, YS ;
Sung, JY ;
Kim, OS ;
Kim, YJ ;
Hur, KC ;
Kazlauskas, A ;
Rhee, SG .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (14) :10527-10531
[8]   Mitochondrial free radical production and aging in mammals and birds [J].
Barja, G .
TOWARDS PROLONGATION OF THE HEALTHY LIFE SPAN: PRACTICAL APPROACHES TO INTERVENTION, 1998, 854 :224-238
[9]   Current molecular models for NADPH oxidase regulation by Rac GTPase [J].
Bokoch, GM ;
Diebold, BA .
BLOOD, 2002, 100 (08) :2692-2696
[10]   CELLULAR PRODUCTION OF HYDROGEN-PEROXIDE [J].
BOVERIS, A ;
CHANCE, B ;
OSHINO, N .
BIOCHEMICAL JOURNAL, 1972, 128 (03) :617-&