A Network Toxicology Analysis of the Molecular Pathways and Novel Targets in TCDD-Induced Cardiovascular Toxicity

Abstract

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant, disrupt multiple systems including endocrine, immun, nervous, reproductive, developmental, and cardiovascular. This study aimed to identify the molecular pathways and potential therapeutic targets for TCDD-induced cardiovascular toxicity using CTD, ShinyGO, STRING, GeneMANIA, ChEA3, MIENTURNET, and Cytoscape computational tools. The analysis identified the AGE-RAGE signaling pathway, blood circulation, and cytokine receptor binding as the top3 among 10 key molecular pathways, biological processes, and molecular functions associated with TCDD-induced cardiovascular toxicity. Additionally, 10 hub proteins/genes were found to play a critical role, with NFKB1 being the most important regulating transcription factor and hsa-miR-19a-3p and hsa-miR-125b-5p as the most crucial microRNAs. This study sheds light on the molecular mechanisms underlying TCDD-induced cardiovascular toxicity, revealing novel potential targets for therapeutic intervention.