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糖尿病患者急性肾损伤向慢性肾脏病转变的炎性因子机制

Review of the Mechanism of Inflammatory Factors in the Transition from Acute Kidney Injury to Chronic Kidney Disease in Diabetes Patients

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糖尿病患者是急性肾损伤(AKI))和慢性肾脏病(CKD)的高危人群.AKI可加速CKD的进展,而CKD又会增加AKI的发生率和严重程度.炎性细胞因子在糖尿病患者AKI向CKD转变中发挥重要作用,但在AKI和CKD中的作用机制有所不同.在AKI早期,促炎性细胞因子,如白细胞介素-1β(IL-1β)、白细胞介素-18(IL-18)、肿瘤坏死因子-α(TNF-α)占主导,加重肾脏损伤;在AKI恢复期或CKD期,促纤维化细胞因子(如TGF-β等)占主导,促进肾间质纤维化.炎性细胞因子可通过诱导肾小管上皮细胞凋亡、上皮-间质转化(EMT)和自噬,内皮-间质转化(EndoMT),以及激活间质细胞分泌基质成分等途径影响肾脏结构和功能.针对炎性细胞因子的干预策略为阻断糖尿病患者由AKI向CKD转变提供了新思路.
Diabetic patients are at high risk of acute kidney injury(AKI)and chronic kidney disease(CKD).AKI can accelerate the progression of CKD,while CKD increases the incidence and severity of AKI.Inflammatory cytokines play an important role in the transition from AKI to CKD in diabetic patients,but their mechanisms differ between AKI and CKD.In the early stage of AKI,pro-inflammatory cytokines(such as IL-1β,IL-18,TNF-α,etc.)predominate and aggravate renal injury;in the recovery stage of AKI or CKD,pro-fibrotic cytokines(such as TGF-β,etc.)predominate and promote renal interstitial fibrosis.Inflammatory cytokines affect renal structure and function by inducing apoptosis,EMT and autophagy of renal tubular epithelial cells,EndoMT of endothelial cells,and activating interstitial cells to secrete matrix components.Interventions targeting inflammatory cytokines provide new insights for blocking the transition from AKI to CKD in diabetic patients.

DiabetesAcute kidney injuryChronic kidney diseaseInflammatory cytokines

高尚刘鑫、朱国贞

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山西医科大学第二医院肾内科,太原 030001

糖尿病 急性肾损伤 慢性肾脏病 炎性细胞因子

2024

微循环学杂志
武汉大学人民医院,中国病理生理学会微循环专业委员会

微循环学杂志

CSTPCD
影响因子:0.969
ISSN:1005-1740
年,卷(期):2024.34(3)