# Mechanistic insights into cadmium-induced hepatotoxicity mediated by dysregulation of microRNA expression

## TL;DR

This study explores how cadmium causes liver damage in mice by disrupting microRNA regulation, leading to inflammation and cell death.

## Contribution

The study identifies miRNA-mediated regulatory mechanisms as potential upstream contributors to cadmium-induced liver injury.

## Key findings

- Cd exposure caused liver injury marked by altered liver function and cellular disruption.
- Differentially expressed miRNAs target genes in inflammation and apoptosis pathways like MAPK and TNF.
- The findings suggest miRNA regulation plays a role in Cd-induced hepatotoxicity.

## Abstract

Cadmium (Cd), a toxic heavy metal pollutant, poses a serious threat to environmental and health and exhibits pronounced hepatotoxicity. However, the underlying mechanisms—particularly those involving microRNA (miRNA) regulation—remain incompletely understood. In this study, an acute liver injury model was established in mice via oral gavage administration of cadmium chloride (18 μg/L, 0.8 mL/day). A comprehensive methodological approach was employed, including serum biochemical assays, histopathological examination, transmission electron microscopy, quantitative Polymerase Chain Reaction acronym (PCR), and high-throughput miRNA sequencing combined with bioinformatic analyses, to systematically investigate the mechanisms of Cd-induced hepatotoxicity. The results demonstrated that Cd exposure led to marked hepatic injury, reflected by altered liver function indices, hepatocellular ultrastructural disruption, apoptosis, and inflammatory responses. However, these downstream pathological changes do not explain how the coordinated inflammatory and apoptotic responses are initiated at the molecular level, highlighting the need to identify upstream regulatory mechanisms. To explore upstream regulatory mechanisms, miRNA transcriptomic analysis indicated that the target genes of differentially expressed miRNAs are enriched in inflammation- and apoptosis-related pathways, including MAPK and TNF signaling. These results suggest a potential role for miRNA-mediated regulation in cadmium-induced liver injury in mice and provide a basis for further investigation of molecular responses to heavy metal exposure.