O. Moe

Publications377
h-index77
Citations21,809
Highly Influential Citations869
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FGF23 induces left ventricular hypertrophy.
TLDR
It is reported that elevated FGF23 levels are independently associated with LVH in a large, racially diverse CKD cohort and suggested that chronically elevated F GF23 levels contribute directly to high rates of LVH and mortality in individuals with CKD.
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Regulation of Fibroblast Growth Factor-23 Signaling by Klotho*
TLDR
It is shown that Klotho protein directly binds to multiple FGF receptors (FGFRs) and significantly enhanced the ability of FGF23 to induce phosphorylation of F GF receptor substrate and ERK in various types of cells.
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Kidney stones: pathophysiology and medical management
  • O. Moe
  • Medicine, Biology
    The Lancet
  • 28 January 2006
View on Elsevier
Klotho deficiency causes vascular calcification in chronic kidney disease.
TLDR
Klotho is an early biomarker for CKD, and Klotho deficiency contributes to soft-tissue calcification in CKD.
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Fibroblast growth factor 23 and Klotho: physiology and pathophysiology of an endocrine network of mineral metabolism.
TLDR
This review covers recent data on the physiological regulation and function of the complex FGF23-αKlotho network.
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Expression of NHE-3 in the apical membrane of rat renal proximal tubule and thick ascending limb.
TLDR
NHE-3 is the isoform responsible for NaCl and NaHCO3 absorption in the proximal convoluted tubule, and NahCO absorption in a thick ascending limb and apical membrane Na/H exchange activity is likely mediated by other isoform of the NHE family.
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Klotho: a novel phosphaturic substance acting as an autocrine enzyme in the renal proximal tubule
TLDR
Klotho is a novel phosphaturic substance that acts as an enzyme in the proximal tubule urinary lumen by modifying glycans, which cause decreased transporter activity, followed by proteolytic degradation and possibly internalization of NaPi‐2a from the apical membrane.
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Acute Inhibition of Na/H Exchanger NHE-3 by cAMP
TLDR
It is concluded that regulation of NHE-3 by PKA in vivo involves complex mechanisms, which include phosphorylation of Ser-552 and Ser-605, which were phosphorylated in vivo.
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Global kidney health 2017 and beyond: a roadmap for closing gaps in care, research, and policy
View on Elsevier
Klotho deficiency is an early biomarker of renal ischemia-reperfusion injury and its replacement is protective.
TLDR
It is found that ischemia-reperfusion injury (IRI) in rodents reduced Klotho in the kidneys, urine, and blood, all of which were restored upon recovery from AKI.
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