| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Outline of Final Research Achievements |
The development of tubulointerstitial lesions is closely correlated with the progressive decline in renal function in diabetic nephropathy (DN). The aim of this study was to clarify the influential role of cellular iron metabolism in the process of tubular injury in DN. We observed an increased expression of the iron-importing transport proteins [transferrin receptor 1 (TfR1) and divalent metal transporter 1 (DMT1)], while a decreased expression of the mitochondrial iron chaperone, Frataxin, accompanied the decline of manganese superoxide dismutase (MnSOD) activity in isolated proximal tubules from the db/db mouse, a model of type II DN. These findings suggest that the dysregulations of cellular iron transport as well as mitochondrial iron metabolism including antioxidative functions within proximal tubules in DN could contribute to the pathophysiology of the progressive tubulointerstitial damage.
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