Probing the microRNA landscape in cadmium chloride induced renal toxicity through an in silico approach.

Cadmium chloride (CdCl₂), a highly toxic environmental pollutant, significantly impacts kidney health, particularly in the proximal tubular cells, where it induces oxidative stress and lipid peroxidation. The specific mechanisms underlying cadmium toxicity remain unclear. It is hypothesized that it is mediated by microRNAs (miRNAs). These non-coding RNAs regulate gene expression by promoting mRNA degradation and translational repression. In this study, microarray data from HK-2 cells exposed to CdCl₂ was analyzed, revealing increased oxidative stress and disrupted mitochondrial function. The prolonged cadmium exposure disrupted gene expression and induced persistent toxicity. Notably, six miRNAs predominantly modulated the hub genes. A molecular interaction study of miRNA-mRNA duplexes indicated a strong interaction with the argonaute (AGO) protein of the RNA-induced silencing complex (RISC), suggesting that miRNA-mediated gene silencing plays a crucial role in cadmium-induced renal damage. These findings highlight the critical role of miRNAs in modulating cadmium toxicity and suggest their potential as biomarkers for cadmium-induced renal dysfunction.