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首页> 外文期刊>Journal of inflammation. >Role of inflammation in túbulo-interstitial damage associated to obstructive nephropathy
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Role of inflammation in túbulo-interstitial damage associated to obstructive nephropathy

机译:炎症在阻塞性肾病相关的肾小管间质损伤中的作用

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Obstructive nephropathy is characterized by an inflammatory state in the kidney, that is promoted by cytokines and growth factors produced by damaged tubular cells, infiltrated macrophages and accumulated myofibroblasts. This inflammatory state contributes to tubular atrophy and interstitial fibrosis characteristic of obstructive nephropathy. Accumulation of leukocytes, especially macrophages and T lymphocytes, in the renal interstitium is strongly associated to the progression of renal injury. Proinflammatory cytokines, NF-κB activation, adhesion molecules, chemokines, growth factors, NO and oxidative stress contribute in different ways to progressive renal damage induced by obstructive nephropathy, as they induce leukocytes recruitment, tubular cell apoptosis and interstitial fibrosis. Increased angiotensin II production, increased oxidative stress and high levels of proinflammatory cytokines contribute to NF-κB activation which in turn induce the expression of adhesion molecules and chemokines responsible for leukocyte recruitment and iNOS and cytokines overexpression, which aggravates the inflammatory response in the damaged kidney. In this manuscript we revise the different events and regulatory mechanisms involved in inflammation associated to obstructive nephropathy.
机译:阻塞性肾病的特征是肾脏中的炎症状态,这种状态由受损的肾小管细胞,浸润的巨噬细胞和成肌纤维细胞产生的细胞因子和生长因子促进。这种炎性状态有助于阻塞性肾病的肾小管萎缩和间质纤维化。肾间质中白细胞(尤其是巨噬细胞和T淋巴细胞)的积累与肾损伤的进展密切相关。促炎细胞因子,NF-κB活化,黏附分子,趋化因子,生长因子,NO和氧化应激以不同方式对阻塞性肾病引起的进行性肾损害作出贡献,因为它们诱导白细胞募集,肾小管细胞凋亡和间质纤维化。血管紧张素II产生增加,氧化应激增加和促炎细胞因子的高水平有助于NF-κB活化,进而诱导负责白细胞募集的粘附分子和趋化因子的表达以及iNOS和细胞因子的过表达,从而加重了受损肾脏的炎症反应。在本手稿中,我们修订了与阻塞性肾病相关的炎症中涉及的不同事件和调节机制。

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