Molybdenum exposure causes abnormalities in oxidative phosphorylation metabolism and leads to damage in cardiac energy metabolism

The health risks associated with exposure to molybdenum (Mo) are drawing increasing attention. However, its toxic mechanisms, particularly the impact on cardiac energy metabolism, remain an area of gap in research. In this study, we employed a multi-omics approach to explore in depth the impact of Mo exposure on cardiac energy metabolism. Our research results indicate that Mo exposure leads to cardiac energy metabolism damage and affects the animals' activity levels. A multi-omics joint analysis revealed a regulatory network composed of 6 interconnected metabolic pathways, with oxidative phosphorylation as its core. Among the key molecular players, inorganic pyrophosphatase and short-chain specific acyl-CoA dehydrogenase were identified as critical enzymes involved in ATP production. Additionally, succinate emerged as a central metabolite within the network and may serve as a potential biomarker for heavy metal-induced cardiac energy metabolic dysfunction. This study reveals the latent cardiac risks associated with Mo exposure and provides an organ-specific perspective for the health risk assessment of environmental pollutants.