Sho Hasegawa

Mild elevation of urinary biomarkers in prerenal acute kidney injury.

Dietary Metabolites and Chronic Kidney Disease.

Persistent expression of neutrophil gelatinase-associated lipocalin and M2 macrophage markers and chronic fibrosis after acute kidney injury.

Hypoxia-inducible factor stabilizers for treating anemia of chronic kidney disease.

Comprehensive three-dimensional analysis (CUBIC-kidney) visualizes abnormal renal sympathetic nerves after ischemia/reperfusion injury.

The oral hypoxia-inducible factor prolyl hydroxylase inhibitor enarodustat counteracts alterations in renal energy metabolism in the early stages of diabetic kidney disease.

Vagus nerve stimulation even after injury ameliorates cisplatin-induced nephropathy via reducing macrophage infiltration.

Activation of Sympathetic Signaling in Macrophages Blocks Systemic Inflammation and Protects against Renal Ischemia-Reperfusion Injury.

Harnessing Metabolomics to Describe the Pathophysiology Underlying Progression in Diabetic Kidney Disease.

Decreased IFT88 expression with primary cilia shortening causes mitochondrial dysfunction in cisplatin-induced tubular injury.

Lysophosphatidylcholine mediates fast decline in kidney function in diabetic kidney disease.

Activation of α7 nicotinic acetylcholine receptors attenuates monocyte-endothelial adhesion through FUT7 inhibition.

Association Between Diabetes and Major Bleeding Complications of Renal Biopsy.

Organelle Stress and Crosstalk in Kidney Disease.

Anti-aging mechanism of calorie restriction in humans.