Multi-omics study reveals mitochondrial dysfunction and immune dysregulation in human placentas with high microplastic exposure, highlighting potential risks to maternal-fetal health.
Key Points
To characterize microplastic accumulation in human placental tissue and determine the associated molecular alterations across transcriptomic, proteomic, and metabolomic layers.
Quantified microplastics in human placental tissue using pyrolysis–gas chromatography–mass spectrometry and classified tissues into high- and low-burden exposure groups.
Conducted integrated transcriptomic, proteomic, and metabolomic profiling using the DIABLO framework alongside network analysis to identify key molecular hubs.
Placental tissue with high microplastic burden exhibited multi-layer molecular disruptions involving immune dysregulation, antifolate resistance, oxidative stress, and altered purine and lipid metabolism.
Integrative multi-omics modeling identified distinguishing cross-omics features, establishing NDUFS6 as a central hub linking molecular shifts directly to mitochondrial dysfunction.