Aims: We aimed to determine the impact of aging on ischemic acute kidney injury, especially in terms of the pathological mechanisms of kidney and heart crosstalk. Method: The effects of 45 min of unilateral ischemic reperfusion (IR) of the renal artery on the contralateral kidney and heart were histologically assessed in 7-and 40-week-old SD rats after 7 days. Results: Glomerular sclerosis, interstitial fibrosis and numbers of ED1 cells were significantly increased in the contralateral kidneys of the 40-, but not the 7-week-old rats. The numbers of ED1 cells in the heart significantly and similarly increased in both groups, but reactive fibrosis after IR was significant only in the 40-week-old rats. The exaggerated profibrotic response induced by aging seemed to be closely associated with the increased number of ED1 cells in the affected area. Conclusion: Aging could play a major role in exaggerating the pathological processes of inflammation to fibrosis in remote organs including the heart and the nonischemic kidney after IR stimulation of the unilateral kidney.
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