KLOTHO SUPPLEMENTATION AMELIORATES RENAL INJURY IN ALDOSTERONE-SALT HYPERTENSION

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https://storage.unitedwebnetwork.com/files/1099/12046027ebe5a1ece34b689db10b649b.pdf

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KLOTHO SUPPLEMENTATION AMELIORATES RENAL INJURY IN ALDOSTERONE-SALT HYPERTENSION

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Co-author 1

Tsuneo Takenaka takenaka@iuhw.ac.jp International University of Health and Welfare Nephrology Tokyo Japan *

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Introduction

Aldosterone induces senescence in renal tubular cells. Renal expression of klotho, which inhibits insulin-like growth factor (IGF) and transforming growth factor (TGF) β signaling, was reduced in aldosterone-salt hypertension (ASH).

Methods

In the present study, we assessed whether klotho protein supplementation is reno-protective in ASH rats. Human recombinant klotho (30 µg/kg/day) was given daily by subcutaneous injection for 4 weeks.

Results

Compared to the controls, blood pressure, albuminuria, isoprostane excretion, glomerular filtration rate (GFR), glomerular cellularity, fibrosis index, renal angiotensin II (ANGII) level, renal expressions of p21 and PTEN-induced kinase 1 (PINK1) were elevated in ASH rats. In contrast, renal expression of mitochondrial transcription factor A (TFAM), superoxide dismutase (SOD) and klotho were reduced in ASH rats, compared to the controls. Klotho supplementation to ASH rats attenuated the increments of blood pressure, albuminuria, isoprostane excretion, GFR, glomerular cellularity, fibrosis index, renal ANGII level, renal expressions of p21 and PINK1. Klotho supplementation reversed the decrements of renal expression of TFAM, SOD and klotho in ASH rats.

Conclusion

The present data indicated that klotho supplementation decreased GFR, blood pressure and albuminuria at least partly via inactivation of renal renin-angiotensin system in ASH rats. Furthermore, our results provided the evidence that klotho protein supplementation inhibited IGF signals, inducing SOD to attenuate oxidative stress, mesangial proliferation and mitochondrial damage. Finally, the present findings suggest that klotho suppresses TGFβ signals to ameliorate fibrosis and tubular senescence in ASH rats.

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