Changing gears in the course of glomerulonephritis by shifting superoxide to nitric oxide-dominated chemistry.
The glomerular response to injury displays astonishingly uniform features that include infiltration with professional immune cells, activation and proliferation of resident glomerular cells and matrix expansion. Cross-communication of intrinsic mesangial cells with invading immune cells is crucial for the fate of glomerular injury: progression to glomerulosclerosis or resolution and repair. The formation of free radicals, particularly of nitric oxide and superoxide, are key events that initiate redox-based signal transduction and gene expression. The balance between these radicals constitutes redox-operated genetic switches that ensure self-limited inflammatory responses to tissue injury. The aberrant production of the mediators, however, may sustain matrix accumulation and result in irreversible alteration of glomerular structure and function.
Pfeilschifter
Josef
J
Pharmazentrum Frankfurt, Klinikum der Johann Wolfgang Goethe-Universität, Theodor-Stern-Kai 7, D-60590 Frankfurt/Main, Germany. pfielschifter@em.uni-frankfurt.de
Beck
Karl-Friedrich
KF
Eberhardt
Wolfgang
W
Huwiler
Andrea
A
D000818:Animals; D015870:Gene Expression; D005921:Glomerulonephritis / Q000235:genetics / Q000503:physiopathology*; D009569:Nitric Oxide / Q000502:physiology*; D015398:Signal Transduction; D013481:Superoxides / Q000378:metabolism*; D013997:Time Factors
D013481:Superoxides; D009569:Nitric Oxide