In Figure 2, a schematic summary of current evidence implicates products of the 15-lipoxygenase pathway of arachidonic acid metabolism, principally 15-(S)-HETE and LXA4, as endogenous antagonists for the proinflammatory actions of leukotrienes. In this review, we have presented evidence for the pathophysiologic relevance of leukotrienes in glomerular immune injury and the emerging data on the multifaceted, counter-inflammatory actions of 15-lipoxygenase 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, whether they be 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. Imaginative design of molecular tools for the manipulation of these enzyme systems in vivo, however, represents a potentially fruitful area of research toward the attainment of a highly worthwhile goal--the cure of glomerulonephritis.
|Original language||English (US)|
|Number of pages||13|
|Journal||Advances in nephrology from the Necker Hospital|
|State||Published - 1995|
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