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Relationship between oxidative stress and inflammatory cytokines in diabetic nephropathy

机译：糖尿病肾病中氧化应激与炎性细胞因子的关系

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The prevalence of diabetes has dramatically increased worldwide due to the vast increase in the obesity rate. Diabetic nephropathy is one of the major complications of type 1 and type 2 diabetes and it is currently the leading cause of end-stage renal disease. Hyperglycemia is the driving force for the development of diabetic nephropathy. It is well known that hyperglycemia increases the production of free radicals resulting in oxidative stress. While increases in oxidative stress have been shown to contribute to the development and progression of diabetic nephropathy, the mechanisms by which this occurs are still being investigated. Historically, diabetes was not thought to be an immune disease; however, there is increasing evidence supporting a role for inflammation in type 1 and type 2 diabetes. Inflammatory cells, cytokines, and profibrotic growth factors including transforming growth factor-β (TGF-β), monocyte chemoattractant protein-1 (MCP-1), connective tissue growth factor (CTGF), tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-18 (IL-18), and cell adhesion molecules (CAMs) have all been implicated in the pathogenesis of diabetic nephropathy via increased vascular inflammation and fibrosis. The stimulus for the increase in inflammation in diabetes is still under investigation; however, reactive oxygen species are a primary candidate. Thus, targeting oxidative stress-inflammatory cytokine signaling could improve therapeutic options for diabetic nephropathy. The current review will focus on understanding the relationship between oxidative stress and inflammatory cytokines in diabetic nephropathy to help elucidate the question of which comes first in the progression of diabetic nephropathy, oxidative stress, or inflammation.
机译：由于肥胖率的大量增加，全世界的糖尿病患病率急剧增加。糖尿病肾病是1型和2型糖尿病的主要并发症之一，目前是终末期肾脏疾病的主要原因。高血糖是糖尿病性肾病发展的驱动力。众所周知，高血糖会增加自由基的产生，从而导致氧化应激。虽然氧化应激的增加已被证明有助于糖尿病性肾病的发展和进展，但其发生的机制仍在研究中。从历史上看，糖尿病被认为不是一种免疫疾病。然而，越来越多的证据支持炎症在1型和2型糖尿病中的作用。炎性细胞，细胞因子和纤维化生长因子，包括转化生长因子-β（TGF-β），单核细胞趋化蛋白-1（MCP-1），结缔组织生长因子（CTGF），肿瘤坏死因子-α（TNF-α） ，白介素-1（IL-1），白介素-6（IL-6），白介素-18（IL-18）和细胞黏附分子（CAMs）均与糖尿病性肾病的发病机理有关，其通过增加血管炎症和纤维化。糖尿病炎症增加的刺激作用仍在研究中。但是，活性氧是主要的候选物质。因此，靶向氧化应激-炎性细胞因子信号传导可以改善糖尿病性肾病的治疗选择。本篇综述将集中于了解糖尿病性肾病中氧化应激与炎性细胞因子之间的关系，以帮助阐明哪个问题首先出现在糖尿病性肾病，氧化应激或炎症中。

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