Numerous research studies have been dedicated to investigating diabetic nephropathy (DN), encompassing investigations into molecular signaling and clinical outcomes. It is widely acknowledged that the pathophysiology of DN is influenced by multiple factors. Circular RNAs (circRNAs) are a type of endogenous RNAs distinguished by their covalent loop structure. The primary mechanism by which circRNAs exert their effects is through their sponging activity towards microRNAs. The involvement of circRNAs in the progression of DM has been confirmed, suggesting their potential as innovative biomarkers and therapeutic tools. In this study, a total of 75 diabetic instances were divided into 3 groups equally depending on their albuminuric state, as documented: Normo-albuminuric, Micro-albuminuric and Macro-albuminuric in addition to 25 healthy individuals as controls were involved. We measured Hsa-miR-483-3p, Hsacirc₀123190 and Apelin receptor (APLNR) mRNA gene expressions utilizing quantitative RT-PCR. In addition, Serum levels of APLN (Apelin), Histone deacetylase 1 (HDAC1), Nuclear factor-ΚB (NF-κB), Chemoattractant protein-1 (MCP-1), PUMA, p53 upregulated modulator of apoptosis, transforming growth factor β (TGFβ) and Vascular cell adhesion molecule 1 (VCAM1) had been evaluated by ELISA technique. The work documented significantly down-regulation of Hsacirc₀123190 and APLNR expressions in DN patients compared controls with the lowest level of expression exhibited in macroalbuminuria diabetic group. Whereas a significant up-regulation of Hsa-miR-483-3p expression had been detected in diabetic groups particularly diabetic patients with macroalbuminuria. Parallel findings had been observed concerning serum HDAC1, MCP1, NF-κB, PUMA, p53, TGFβ as well as VCAM1. The work documented the forthcoming impact of Hsacirc₀123190 in progression of DN via its three various stages; By emphasizing its function as a dependable biomarker, this study aims to further the understanding of DN pathogenesis.
Atef et al. (Mon,) studied this question.