title: Changing gears in the course of glomerulonephritis by shifting superoxide to nitric oxide-dominated chemistry.
abstract: 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.
authors.affiliation: Pharmazentrum Frankfurt, Klinikum der Johann Wolfgang Goethe-Universität, Theodor-Stern-Kai 7, D-60590 Frankfurt/Main, Germany. pfielschifter@em.uni-frankfurt.de
authors.forename: Josef
authors.initials: J
authors.lastname: Pfeilschifter
authors.forename: Karl-Friedrich
authors.initials: KF
authors.lastname: Beck
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Eberhardt
authors.forename: Andrea
authors.initials: A
authors.lastname: Huwiler
mesh_terms: 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
chemical_list: D013481:Superoxides; D009569:Nitric Oxide