ArticleCureus2024
Indoxyl Sulfate and Its Potential Role in Mineralocorticoid Receptor Transactivation in Chronic Kidney Disease.
Article in Cureus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 authors.
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Abstract
backgroundThe uremic toxin indoxyl sulfate (IS) is an important factor in chronic kidney disease (CKD) progression. Inhibitors of the renin-angiotensin system and add-on therapy with mineralocorticoid receptor (MR) antagonists can help reduce proteinuria and suppress CKD progression. However, the association between IS and MR activation remains unknown. MATERIALS AND
methods
resultsIn the 5/6 nephrectomy model, the serum IS concentration was significantly increased; however, the plasma aldosterone levels were decreased. Immunohistochemistry showed that the expression of IS protein increased in injured tubular cells in the 5/6 nephrectomy group compared with that in the sham group. Furthermore, evaluations of serial kidney sections revealed that the expression site of IS protein was colocalized with the distal nephron, where the expression of MR protein was observed. MR-mediated transcriptional activity in COS-7 cells was increased in an aldosterone concentration-dependent manner. IS increased MR-mediated transcriptional activity and protein levels with and without aldosterone, and α-lipoic acid attenuated this increase.
conclusionsIS could enhance MR transactivation by increasing MR protein levels through oxidative stress in CKD rats, indicating that treatment with MR antagonists and antioxidants may play a permissive role in inhibiting IS-induced CKD progression.
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