Abstract

Long non-coding RNA taurine upregulated gene 1 plays an important role in the progression of diabetic nephropathy. Studies have shown that there is a complex and precise interaction between taurine upregulated gene 1 and microRNA-22-3p. MicroRNA-22-3p is an important microRNA whose expression level is closely associated with the development and progression of diabetic nephropathy. Through analysis, research has shown that the expression level of microRNA-22-3p is significantly downregulated in patients with diabetic nephropathy, while the high expression of taurine upregulated gene 1 is closely related to the clinical course of diabetic nephropathy. Further studies revealed a negative regulatory mechanism between taurine upregulated gene 1 and microRNA-22-3p. Taurine upregulated gene 1 was able to promote microRNA-22-3p degradation, thereby affecting the biological function of microRNA-22-3p. One of the main intracellular targets of microRNA-22-3p is thioredoxin. Thioredoxin has important physiological functions in redox processes, while its expression level is often regulated in diabetic nephropathy. MicroRNA-22-3p has been shown to inhibit the expression of thioredoxin by directly binding to the 3’ untranslated region of thioredoxin, thereby affecting redox balance and promoting apoptosis and dysfunction in cells. Further studies revealed the regulatory mechanism of taurine upregulated gene 1/microRNA-22-3p/CSE axis in diabetic nephropathy. Taurine upregulated gene 1 modulates the control of thioredoxin by microRNA-22-3p through its influence on microRNA-22-3p expression levels. Elevated taurine upregulated gene 1 expression results in reduced microRNA-22-3p levels, subsequently increasing thioredoxin expression. This cascade helps maintain cellular redox balance, mitigating apoptosis and functional deficits. Overall, long non-coding RNA taurine upregulated gene 1 is involved in important regulatory mechanisms during diabetic nephropathy development by regulating the activity of the microRNA-22-3p/thioredoxin axis. This finding not only contributes to an in-depth understanding of the pathophysiological mechanisms of diabetic nephropathy, but also lays the groundwork for future therapeutic strategies by identifying new theoretical bases and potential therapeutic targets.