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学科主题: 肾脏病学
题名:
急性肾损伤发病与修复的机制
其他题名: Mechanisms of injury and repair of acute kidney injury
作者: 杨莉
关键词: 急性肾损伤 ; 修复 ; 肾小管上皮 ; 微血管 ; 炎症 ; Acute kidney injury ; Repair ; Renal tubular epithelium ; Microvessels ; Inflammation
刊名: 中华肾病研究电子杂志
发表日期: 2013
DOI: 10.3877/cma.j.issn.2095-3216.2013.03.003
期: 3, 页:120-124
文章类型: Journal Article
摘要: 急性肾损伤(AKI)的组织损伤与修复过程由复杂的多种机制、多种效应细胞共同参与。肾小管上皮、微血管内皮和炎症细胞是这一复杂体系的三个关键环节。肾小管上皮细胞是急性损伤的主要靶细胞,通过分泌多种细胞因子调控免疫炎症反应,其增殖障碍直接导致纤维化的发生与发展;微血管内皮损伤后不仅参与炎症反应的发生和发展,其修复不良还导致组织持续缺血缺氧,促进纤维化的发生;AKI后持续免疫炎症反应的失调特别是单核巨噬的持续活化亦为AKI后修复不良的重要因素。 The renal tubular epithelium, the endothelium of microvessels and the inflammatory cells are the three major components of the complicated mechanisms that are involved in the process of tissue injury and repair during acute kidney injury (AKI). The renal tubular epithelial cells are not only the major target of injury, but also modulate inflammatory responses through secreting various cytokines. The maladaptive repair of tubular epithelial cells after AKI initiates interstitial fibrosis. The continuous loss of endothelium of microvessels induces chronic ischemia and hypoxia in the tubulointerstitial compartment, which promotes the progression of fibrosis. The sustained activation of monocytes/macrophages also devotes to the process of fibrosis.
语种: 中文
原文出处: 查看原文
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内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/46058
Appears in Collections:北京大学第一临床医学院_肾脏内科_期刊论文

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作者单位: 100034,北京大学第一医院肾病科北京大学肾脏病研究所

Recommended Citation:
杨莉. 急性肾损伤发病与修复的机制[J]. 中华肾病研究电子杂志,2013(3):120-124.
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