Ischemia/reperfusion of unilateral kidney exaggerates aging-induced damage to the heart and contralateral kidney.

Nephron Experimental Nephrology Pub Date : 2014-01-01 Epub Date: 2014-07-03 DOI:10.1159/000362555

Junichiro Kato, Masaaki Nakayama, Wan-Jun Zhu, Takashi Yokoo, Sadayoshi Ito

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引用次数: 12

Abstract

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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单侧肾脏缺血/再灌注加重了衰老对心脏和对侧肾脏的损伤。

目的:探讨衰老对缺血性急性肾损伤的影响，特别是肾心串扰的病理机制。方法:观察7、40周龄SD大鼠单侧肾动脉缺血再灌注45min对对侧肾脏和心脏的影响。结果:40周龄大鼠对侧肾脏肾小球硬化、间质纤维化及ED1细胞数量明显增加，7周龄大鼠对侧肾脏无明显差异。两组心脏中ED1细胞的数量均显著增加，但仅在40周龄大鼠中，IR后的反应性纤维化显著增加。衰老诱导的过度纤维化反应似乎与患处ED1细胞数量的增加密切相关。结论:单侧肾脏IR刺激后，衰老在心脏、非缺血肾等远端器官炎症到纤维化的病理过程中起重要作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Nephron Experimental Nephrology 医学-泌尿学与肾脏学

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>12 weeks