糖尿病肾病慢性炎症机制研究进展

Progress in the Study of Chronic Inflammatory Mechanism of Diabetic Nephropathy

随着对糖尿病肾病(DKD)研究的不断深入,慢性炎症状态的地位越来越凸显。近年来,一种与天冬氨酸半胱氨酸蛋白水解酶(Caspase)-1相关的程序性细胞死亡机制,通过足细胞与肾小管上皮细胞的焦亡引起一系列炎症反应,最终导致肾功能恶化。肠道菌群异常在慢性肾脏病患者中致病证据越来越充分,其机制表现为菌群比例的失调(有害细菌增多、有益菌减少甚至缺如),产生炎症因子及氧化应激产物。另外,内脂素(Visfatin)在DKD发生发展中均发挥作用,参与胰岛素抵抗、调控糖脂代谢、增强炎症反应等过程。同样,适应性免疫系统及相关细胞因子同样有重要作用,通过T细胞、B细胞及白细胞介素(interleukin, IL)-17A、白细胞介素(interleukin, IL)-2、肿瘤坏死因子(TNF)和肿瘤坏死因子(TNF)受体等细胞因子共同导致蛋白尿的产生、肾功能的恶化。因此,了解诱导慢性炎症的各类分子机制在糖尿病肾病发生以及发展中的作用,对糖尿病肾病的早期识别及治疗有重要意义。

With the continuous deepening of the study of Diabetic Kidney Disease (DKD), the status of chronic inflammation is becoming more and more prominent. In recent years, a programming cell death mechanism related to cyspase-1 is caused by the scorching of foot cells and renal tubular epithelial cells, which causes a series of inflammatory reactions and eventually leads to kidney function worsen. The inferior of the intestinal flora is increasingly sufficient in patients with chronic kidney disease, and its mechanism is manifested as the disorders of the flora ratio (increasing harmful bacteria, reduced beneficial bacteria, or even lack of), producing inflammatory factor and oxidation stimulating products. In addition, Visfatin played a role in the development of DKD to participate in the process of participating in insulin resistance, regulating sugar fat metabolism, and enhancing inflammatory response. Similarly, the adaptive immune system and related cytokine also have an important role, T cells, B cells and cytokines such as interleukin (IL)-17A, interleukin (IL)-2, tumor necrosis factor (TNF) and tumor necrosis factor (TNF) receptor jointly lead to the production of pro-teinuria and the deterioration of renal function. Therefore, understanding the role of various types of molecular mechanisms that induce chronic inflammation in the occurrence and development of diabetic nephropathy is of great significance for the early identification and treatment of diabetic nephropathy.