Cu(OH)2 nanopesticide triggered heart failure-like pathogenesis in mice by potentially targeting mmu-miRNA-590-3p and mmu-miRNA-338-5p in Wnt/β-catenin signaling
摘要
Nanopesticides have been progressively incorporated into contemporary agricultural systems owing to their distinctive physicochemical characteristics and superior pest management capabilities. Given their environmental persistence and propensity for bioaccumulation, nanopesticides are increasingly recognized as emerging cardiovascular toxicants, thus warranting systematic investigation of their exposure-associated cardiotoxic effects.
MethodsIn the present study, the impact of Cu(OH)2 nanopesticide on cardiac homeostasis was systematically investigated in a C57BL/6 mouse model following one-month exposure administered via oral gavage, with copper concentrations set at 0 (vehicle control), 1, and 5 mg/kg bw. Multiple molecular biology techniques were employed to elucidate the nanopesticide-induced cardiac impairment and the underlying mechanisms.
ResultsIt was demonstrated that prolonged exposure to this copper-based nanopesticide resulted in significant deterioration of ventricular systolic and diastolic function, induction of ventricular chamber remodeling, disturbance of hemodynamic stability, and dysregulation of cardiac substructural gene expression, collectively mirroring the characteristic phenotypic manifestations and underlying molecular hallmarks of clinical heart failure. The dysregulation of Cu(OH)2 nanopesticide in the Wnt/β-catenin signaling pathway through the targeting of mmu-miRNA-590-3p and mmu-miRNA-338-5p provided a proposed explanation for the underlying mechanism of the nanopesticide-induced imbalance of cardiac homeostasis.
ConclusionThe present findings provide new insights into the cardiovascular hazards posed by Cu(OH)2 nanopesticide, advancing the development of a more rigorous risk assessment protocol for this emerging category of agricultural nanomaterial.
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