炎症关系:糖尿病肾病的血清淀粉样蛋白A和炎症

R. Anderberg, B. Dieter, R. Meek, K. Tuttle
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引用次数: 1

摘要

炎症在糖尿病肾病(DKD)的进展中起着重要作用,但对这些炎症事件的根本原因知之甚少。血清淀粉样蛋白A (SAA)在多种组织中引发强烈的炎症反应,并在糖尿病肾脏的肾小球和小管间质室中上调。在炎症条件下,足细胞与其他内在细胞一起在肾脏局部产生SAA。我们最近的研究表明,SAA在培养的足细胞中诱导NF-κB活化和随后的炎症趋化因子和细胞因子。最近的证据表明,糖尿病中SAA的局部产生可能导致单核细胞和巨噬细胞募集、中性粒细胞激活和其他相关事件,导致肾脏持续的慢性炎症,这可能进一步加剧DKD。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
An Inflammatory Nexus: Serum Amyloid A and inflammation in Diabetic Kidney Disease
Inflammation contributes a significant part to the advancement of diabetic kidney disease (DKD), yet relatively little is known about the root cause of these inflammatory events. Serum Amyloid A (SAA) triggers a potent inflammatory response in a variety of tissues and is up-regulated in glomerular and tubulointerstitial compartments of the diabetic kidney. Under inflammatory conditions, podocytes, along with other intrinsic cells, produce SAA locally in the kidney. Our recent work has shown that SAA induces NF-κB activation and subsequent inflammatory chemokines and cytokines in cultured podocytes. Recent evidence suggests that local production of SAA in diabetes may lead to monocyte and macrophage recruitment, neutrophil activation, and other related incidents resulting in sustained chronic inflammatory conditions in the kidney which may further exacerbate DKD.
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