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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.
Cardiovascular toxicity hsa-miR-19a-3p hsa-miR-125b-5p NFKB1 TCDD
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Birincil Dil | İngilizce |
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Konular | Toksikoloji |
Bölüm | Araştırma Makalesi |
Yazarlar | |
Proje Numarası | - |
Yayımlanma Tarihi | 25 Ağustos 2024 |
Gönderilme Tarihi | 22 Nisan 2024 |
Kabul Tarihi | 19 Temmuz 2024 |
Yayımlandığı Sayı | Yıl 2024 |