Title : Klotho modulates FGF23-mediated NO synthesis and oxidative stress in human coronary artery endothelial cells.

Pub. Date : 2016 Sep

PMID : 27448998






4 Functional Relationships(s)
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1 Pre-incubation with a Klotho inhibitor blunts the FGF23-stimulated Akt-eNOS activation and NO synthesis, and decreases ROS degradation by blocking SOD2 and CAT enzymes, whereas FGF23-stimulated ROS synthesis via Nox2 is unaffected, resulting in low NO bioavailability and increased oxidative stress. Reactive Oxygen Species klotho Homo sapiens
2 Pre-incubation with a Klotho inhibitor blunts the FGF23-stimulated Akt-eNOS activation and NO synthesis, and decreases ROS degradation by blocking SOD2 and CAT enzymes, whereas FGF23-stimulated ROS synthesis via Nox2 is unaffected, resulting in low NO bioavailability and increased oxidative stress. Reactive Oxygen Species klotho Homo sapiens
3 In states of Klotho deficiency, e.g., CKD, FGF23-mediated NO synthesis is blunted and ROS formation overrules ROS degradation. Reactive Oxygen Species klotho Homo sapiens
4 In states of Klotho deficiency, e.g., CKD, FGF23-mediated NO synthesis is blunted and ROS formation overrules ROS degradation. Reactive Oxygen Species klotho Homo sapiens