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10.1053/j.ajkd.2011.03.029

http://scihub22266oqcxt.onion/10.1053/j.ajkd.2011.03.029
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C4792515!4792515!21705125
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suck abstract from ncbi


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pmid21705125      Am+J+Kidney+Dis 2011 ; 58 (3): 471-9
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  • Aldosterone Induced Fibrosis in the Kidney: Questions and Controversies #MMPMID21705125
  • Brem AS; Morris DJ; Gong R
  • Am J Kidney Dis 2011[Sep]; 58 (3): 471-9 PMID21705125show ga
  • Over the years, aldosterone has been a favorite topic of renal physiologists given its role in the maintenance of the body fluids. Investigators are only recently coming to appreciate a second pro-inflammatory and pro-fibrotic role for this hormone. Mineralocorticoids, like aldosterone, trigger a pro-fibrotic process, which in many respects mimics the early phase of wound healing. Depending on the type of cell involved, aldosterone may activate the pro-fibrotic process through classical mineralocorticoid receptors (MR), non-classical membrane associated MR, and/or glucocorticoid receptors. In the kidney, the actions of aldosterone can be attenuated by 11-dehydro metabolites of endogenous glucocorticoids generated by isoforms of the enzyme 11?-hydroxysteroid dehydrogenase (11?-HSD-1 and 11?-HSD-2). Thus the renal 11?-HSD isoforms may have two functions; to prevent endogenous glucocorticoids from inappropriately binding to and activating MR and to synthesize agents that limit the actions of aldosterone. While sodium in the diet has been implicated in aggravating aldosterone induced renal fibrotic processes, preliminary findings are consistent with the view that aldosterone alone can initiate the matrix production in renal tissue even in the absence of active sodium transport. Thus, there is a growing body of laboratory and clinical evidence supporting the use of inhibitors of aldosterone action in patients with both glomerular and tubular diseases.
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