Publications by authors named "Aya Yagi-Tomita"

Article Synopsis
  • Streptozotocin (STZ) is mainly used as an anti-cancer drug for treating neuroendocrine tumors (NETs) but can also cause DNA damage in kidney cells, leading to injury.
  • Research showed that this kidney damage is linked to the activation of the p53 signaling pathway and reduced membrane transporters in tubular epithelial cells.
  • Treatment with an SGLT2 inhibitor can help protect kidney cells from STZ-induced damage without affecting the drug's effectiveness on pancreatic β-cells, suggesting its potential as a preventative treatment for kidney injury in NET patients.
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Based on recent clinical trials using sodium-glucose co-transporter 2 inhibitor (SGLT2i) demonstrating the significant improvement of outcomes of diabetic kidney disease (DKD), the paradigm shift from "glomerulocentric" to "tubule centric" pathophysiology in DKD progression has been highlighted. Several responsible mechanisms for renoprotective effects by SGLT2i have been proposed recently, but the changes in proximal tubule-specific gene expression by SGLT2i in diabetic mice have not been elucidated. We report the analysis of the proximal tubular-specific pathway, demonstrating the downregulation of oxidative phosphorylation in dapagliflozin-treated mice, a type 2 diabetic model.

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Kidney hypertrophy is a common clinical feature in patients with diabetes and is associated with poor renal outcomes. Initial cell proliferation followed by cellular hypertrophy are considered the responsible mechanisms for diabetic kidney hypertrophy. However, whether similar responses against hyperglycemia continue in the chronic phase in diabetes is unclear.

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Article Synopsis
  • Heart failure often leads to kidney failure, and when both occur together, they significantly increase mortality rates in patients.
  • Recent research indicates that kidney injury in heart failure patients is primarily due to increased kidney venous pressure rather than just reduced blood flow from the heart.
  • A new mouse model study found that decreased blood flow in kidney capillaries, caused by kidney congestion and activated NF-κB signaling, worsens kidney damage, suggesting that targeting NF-κB could be a promising treatment for paired heart and kidney failures.
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