Publications by authors named "Yuri Kasagi"

Article Synopsis
  • Pseudohypoaldosteronism type II (PHAII) is a hereditary condition linked to mutations in genes like CUL3, leading to the decreased degradation of WNK proteins, which contributes to hypertension.
  • A study using mice with a specific CUL3 mutation revealed a PHAII-like phenotype and significantly reduced levels of KLHL3, a protein crucial for linking WNKs to CUL3, while other KLHL family proteins remained unchanged.
  • The findings suggest that the reduction of KLHL3 specifically results from the CUL3 mutation, enhancing our understanding of the disease's underlying mechanisms.
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Article Synopsis
  • The Keap1-Nrf2-ARE signaling pathway is crucial for protecting cells from oxidative stress by regulating the expression of cytoprotective enzymes.
  • Researchers aimed to disrupt the interaction between Keap1 and Nrf2 to elevate Nrf2 expression and enhance the antioxidant response.
  • By screening 1,633 drugs through a new fluorescence correlation spectroscopy system, they identified 12 candidates, with 2 notably increasing Nrf2 levels and upregulating related gene activity in liver cells.
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Muscle wasting or sarcopenia contributes to morbidity and mortality in patients with cancer, renal failure, or heart failure, and in elderly individuals. Na-K-2Cl cotransporter 1 (NKCC1) is highly expressed in mammalian skeletal muscle, where it contributes to the generation of membrane ion currents and potential. However, the physiologic function of NKCC1 in myogenesis is unclear.

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Mutations in the with-no-lysine kinase 1 (WNK1), WNK4, Kelch-like 3 (KLHL3), and Cullin3 (CUL3) genes were identified as being responsible for hereditary hypertensive disease pseudohypoaldosteronism type II (PHAII). Normally, the KLHL3/CUL3 ubiquitin ligase complex degrades WNKs. In PHAII, the loss of interaction between KLHL3 and WNK4 increases levels of WNKs because of impaired ubiquitination, leading to abnormal over-activation of the WNK-OSR1/SPAK-NCC cascade in the kidney's distal convoluted tubules (DCT).

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Background: Renal anemia of chronic kidney disease (CKD) is generally treated by erythropoiesis-stimulating agents (ESAs). However, there are individual differences in patients' responsiveness to ESA, which may affect the prognosis of CKD.

Methods: The effect of ESAs on hemoglobin was followed in 297 CKD patients with renal anemia.

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A 48-year-old man with autosomal dominant polycystic kidney disease (ADPKD) was admitted to our hospital with a 5-day history of lower right back pain, high-grade fever, and arthralgia. He was diagnosed with right kidney cyst infection and bacteremia due to Helicobacter cinaedi (H. cinaedi) based on these symptoms, highly elevated CRP (32.

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Background: Hyponatremia is associated with increased mortality in chronic kidney disease with and without end-stage renal disease (ESRD). Increasing evidence suggests that hyponatremia is not only a marker of severe underlying disease, but also a direct contributor to mortality. However, specific pathogenesis or diseases contributing to mortality in the hyponatremic population are unknown.

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