芹菜素通过Sirt3介导线粒体自噬改善糖尿病肾病氧化应激的研究进展
Research Progress on Apigenin Ameliorating Oxidative Stress in Diabetic Nephropathy via Sirt3-Mediated Mitophagy
DOI: 10.12677/acm.2026.162363, PDF,    科研立项经费支持
作者: 马瑜洁, 丁甜烨, 潘晨晨, 余笑澜:绍兴文理学院医学院,浙江 绍兴;诸葛福媛*:绍兴市人民医院内分泌代谢科,浙江 绍兴
关键词: 芹菜素Sirt3线粒体自噬氧化应激糖尿病肾病Apigenin Sirt3 Mitophagy Oxidative Stress Diabetic Nephropathy
摘要: 糖尿病肾病(DN)是糖尿病常见的微血管并发症,全球患病率持续攀升,其核心病理机制与高血糖诱导的线粒体功能障碍、活性氧(ROS)过度生成及氧化应激密切相关。近年研究发现,线粒体自噬作为选择性清除受损线粒体的关键机制,可通过维持线粒体稳态减轻氧化应激,而沉默调节蛋白3 (Sirt3)作为线粒体核心去乙酰化酶,通过激活Pink1-Parkin增强线粒体自噬,成为DN干预的重要靶点。芹菜素(Apigenin)作为天然黄酮类化合物,具有抗氧化、抗炎及代谢调节特性,研究表明其可通过上调Sirt3表达,促进线粒体自噬并抑制ROS蓄积,从而改善DN模型肾损伤。本综述探讨了芹菜素通过增强Sirt3活性从而促进线粒体自噬对氧化应激产生的影响和对DN潜在的保护机制,为治疗DN的新策略提供了启示。
Abstract: Diabetic nephropathy (DN) is a common microvascular complication of diabetes, with a continuously rising global prevalence. Its core pathological mechanism is closely related to mitochondrial dysfunction induced by hyperglycemia, excessive generation of reactive oxygen species (ROS), and oxidative stress. Recent studies have found that mitochondrial autophagy, as a key mechanism for selectively clearing damaged mitochondria, can alleviate oxidative stress by maintaining mitochondrial homeostasis. Silencing regulatory protein 3 (Sirt3), as a mitochondrial core deacetylase, enhances mitochondrial autophagy by activating Pink1-Parkin and has become an important target for DN intervention. Apigenin, as a natural flavonoid compound, has antioxidant, anti-inflammatory and metabolic regulatory properties. Studies have shown that it can improve renal injury in DN models by up-regulating the expression of Sirt3, promoting mitochondrial autophagy and inhibiting ROS accumulation. This review explores the impact of apigenin on oxidative stress by enhancing Sirt3 activity and thereby promoting mitochondrial autophagy, as well as its potential protective mechanism against DN, providing inspiration for new strategies in the treatment of DN.
文章引用:马瑜洁, 丁甜烨, 潘晨晨, 余笑澜, 诸葛福媛. 芹菜素通过Sirt3介导线粒体自噬改善糖尿病肾病氧化应激的研究进展[J]. 临床医学进展, 2026, 16(2): 73-83. https://doi.org/10.12677/acm.2026.162363

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