Lipoxygenase products as mediators in immune-mediated glomerular injury.
Figure 4 is a schematic summary of current evidence implicating products of the 15-LO pathway of arachidonic acid metabolism, principally 15-(S)-HETE and LXA4, as endogenous antagonists for the proinflammatory actions of LTs. In this article, we have presented evidence for the pathophysiological relevance of LTs in glomerular immune injury, and the emerging data on the multifaceted counter-inflammatory actions of 15-LO products as they relate specifically to the renal glomerulus. Clearly, these concepts are of a broader nature and would be expected to pertain to inflammatory reactions in general, be they in the glomerulus, the renal interstitium, or in extrarenal sites. The extent to which these early observations can be exploited to design strategies for the control of self-destructive inflammatory reactions in the kidney and elsewhere will be determined by future studies.
Takahashi
K
K
Division of Nephrology, Vanderbilt University, Nashville, TN 37232-2372.
Badr
K F
KF
D000818:Animals; D005921:Glomerulonephritis / Q000276:immunology; D006801:Humans; D007678:Kidney Glomerulus / Q000276:immunology* / Q000293:injuries; D015289:Leukotrienes / Q000502:physiology; D008084:Lipoxygenase / Q000378:metabolism*
D015289:Leukotrienes; D008084:Lipoxygenase