Molecular signature of cadmium-mediated neurodevelopmental disorders in prenatal to postnatal stages.

Cadmium can surpass fetal circulation and the blood-brain barrier due to its similar physicochemical properties to those of other divalent metals and causes diverse neuronal disorders. Previous reports have suggested a possible link between epigenetic alterations and neuronal changes in offspring due to cadmium exposure at different developmental stages. Hypermethylation of the glucocorticoid receptor NR3C1 disturbs the development of the hypothalamic-pituitary-adrenal axis, which in turn is responsible for the abnormal cognitive behavior of neonates. In addition, the upregulation of placental miR-509-3p and miR-193-5p expression was found to be the major cause of impaired development of the central nervous system. In this review, the epigenetic mechanism of cadmium-mediated neurotoxicity is described. Moreover, the journey of cadmium from the maternal body to the fetal body through circulation and to the neonatal body through breast milk is also tracked. The vulnerability of developing fetuses to cadmium is an alarming issue. Different types of epigenetic changes, such as DNA methylation, altered miRNA expression and histone modifications, are induced by cadmium and lead to various types of neurodevelopmental disorders. We hope this narrative review will provide distinct knowledge of the transportation of cadmium and its adverse effects on fetal neurodevelopment. See also the graphical abstract(Fig. 1).