Diabetic nephropathy (DN) is a serious complication of diabetes that causes glomerular sclerosis and end-stage renal disease, leading to ascending morbidity and mortality in diabetic patients. Excessive accumulation of aberrantly modified proteins or damaged organelles, such as advanced glycation end-products, dysfunctional mitochondria, and inflammasomes is associated with the pathogenesis of DN. As one of the main degradation pathways, autophagy recycles toxic substances to maintain cellular homeostasis and autophagy dysregulation plays a crucial role in DN progression. MicroRNA (miRNA) and long non-coding RNA (lncRNA) are non-coding RNA (ncRNA) molecules that regulate gene expression and have been implicated in both physiological and pathological conditions. Recent studies have revealed that autophagy-regulating miRNA and lncRNA have been involved in pathological processes of DN, including renal cell injury, mitochondrial dysfunction, inflammation, and renal fibrosis. This review summarizes the role of autophagy in DN and emphasizes the modulation of miRNA and lncRNA on autophagy during disease progression, for the development of promising interventions by targeting these ncRNAs in this disease.

中文翻译：

---

miRNA和lncRNA对糖尿病肾病自噬的调节作用

糖尿病肾病（DN）是糖尿病的一种严重并发症，可导致肾小球硬化和终末期肾病，导致糖尿病患者的发病率和死亡率不断上升。异常修饰的蛋白质或受损的细胞器（例如晚期糖基化终产物、功能失调的线粒体和炎症小体）的过度积累与 DN 的发病机制有关。作为主要的降解途径之一，自噬回收有毒物质以维持细胞稳态，自噬失调在 DN 进展中起着至关重要的作用。 MicroRNA (miRNA) 和长链非编码 RNA (lncRNA) 是调节基因表达的非编码 RNA (ncRNA) 分子，与生理和病理条件有关。最近的研究表明，自噬调节的miRNA和lncRNA参与了DN的病理过程，包括肾细胞损伤、线粒体功能障碍、炎症和肾纤维化。本综述总结了自噬在 DN 中的作用，并强调了 miRNA 和 lncRNA 在疾病进展过程中对自噬的调节，以便通过针对该疾病的这些 ncRNA 来开发有前景的干预措施。