This study investigates the role of miR-203 in regulating renal cell injury in diabetic nephropathy by targeting the suppressor of cytokine signaling (SOCS) proteins SOCS6 and SOCS7. Using NRK cells, we assessed apoptosis through flow cytometry and TUNEL assays, while real-time quantitative PCR (RT-PCR) quantified miRNA and mRNA expressions. Cell viability was measured using the CCK-8 assay, and cytokine levels were determined through ELISA. We also evaluated reactive oxygen species (ROS) and malondialdehyde (MDA) levels with specific assay kits. The dual luciferase assay confirmed the interaction of miR-203 with SOCS6 and SOCS7. Western blotting analyzed the protein levels of key signaling molecules including JAK1, p-JAK1, JAK2, p-JAK2, STAT3, and p-STAT3.Our findings revealed that high glucose (HG) treatment reduced miR-203 levels, leading to decreased NRK cell proliferation, increased cytokine concentrations (TNF-α, IL-1β, IL-4, IL-6), heightened ROS and MDA levels, and increased cell apoptosis. Notably, miR-203 mimics counteracted HG's detrimental effects, while miR-203 inhibitors exacerbated them. Mechanistically, miR-203 directly decreased SOCS6 and SOCS7 expression, thereby inhibiting JAK/STAT3 signaling. Thus, miR-203 provides protective effects against renal cell injury by modulating SOCS and their associated pathways.

In this editorial, we comment on the article by Wu et al published "MicroRNA-630 alleviates inflammatory reactions in rats with diabetic kidney disease by targeting toll-like receptor 4". Diabetic kidney disease (DKD) stands as a significant complication occurring from diabetes mellitus, which contributes substantially to the morbidity and mortality rates worldwide. Renal tubular epithelial cell da-mage, often accompanied by inflammatory responses and mesenchymal trans-differentiation, plays a pivotal role in the progression of DKD. Despite extensive research, the intricate molecular mechanisms underlying these processes remain to be determined. Wu et al remarkable work identifies microRNA-630 (miR-630) as an emerging potential regulator of cell migration, apoptosis, and autophagy, prompting investigation into its association with DKD pathogenesis. This study endeavors to elucidate the impact of miR-630 on TEC injury and the inflammatory response in DKD rats. The role of miR-630 in human DKD will be of interest for future studies.

Diabetic kidney disease (DKD) is one of the complications of diabetes, affecting millions of people worldwide. The relentless progression of this condition can lead to kidney failure, requiring life-altering interventions such as dialysis or transplants. Accumulating evidence suggests that immunologic and inflammatory elements play an important role in initiating and perpetuating the damage inflicted on renal tissues, exacerbating the decline in organ function. Toll-like receptors (TLRs) are a family of receptors that play a role in the activation of the innate immune system by the recognition of pathogen-associated molecular patterns. Recent data from in vitro and in vivo studies have highlighted the critical role of TLRs, mainly TLR2 and TLR4, in the pathogenesis of DKD. In the diabetic milieu, these TLRs recognize diabetic-associated molecular signals, triggering a proinflammatory cascade that initiates and perpetuates inflammation and fibrogenesis in the diabetic kidney. Emerging non-traditional strategies targeting TLR signaling with potential therapeutic implications in DKD have been pro-posed. One of these approaches is the use of microRNAs, small non-coding RNAs that can regulate gene expression. This editorial comments on the results of this approach carried out in a rat model of diabetes by Wu et al, published in this issue of the World Journal of Diabetes. The results of the experimental study by Wu et al shows that microRNA-630 decreased levels compared to non-diabetic rats. Additionally, microRNA-630 exerted anti-inflammatory effects in the kidneys of diabetic rats through the modulation of TLR4. These findings indicate that the microRNA-630/TLR4 axis might represent a pathological mechanism of DKD and a potential therapeutic target capable of curbing the destructive inflammation characteristic of DKD.