Multi-level evidence reveals PANK2 as a potential target of PFOA/PFOS-induced bone metabolism disruption: From network toxicology to in vitro validation

Perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) are two representative per- and polyfluoroalkyl substances (PFAS) that have attracted increasing attention due to their environmental persistence and potential health risks, while their bone toxicity remains unclear. In this study...

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Main Authors: Yiming Shao, Wenhao Fan
Format: Article
Language:English
Published: Elsevier 2025-09-01
Series:Ecotoxicology and Environmental Safety
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Online Access:http://www.sciencedirect.com/science/article/pii/S0147651325009388
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author Yiming Shao
Wenhao Fan
author_facet Yiming Shao
Wenhao Fan
author_sort Yiming Shao
collection DOAJ
description Perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) are two representative per- and polyfluoroalkyl substances (PFAS) that have attracted increasing attention due to their environmental persistence and potential health risks, while their bone toxicity remains unclear. In this study, we systematically investigated the toxicological mechanisms of PFOA and PFOS on bone metabolism by integrating network toxicology, molecular docking and molecular dynamics simulations, and in vitro cellular experiments. Pantothenate kinase 2 (PANK2) was identified as a key target through the intersection of multiple databases and cross-validation using three machine learning algorithms. Molecular docking and dynamics simulations demonstrated that PFOA and PFOS can stably bind to PANK2 protein. In vitro experiments further confirmed that both PFOA and PFOS significantly suppressed PANK2 expression in bone marrow mesenchymal stem cells (BMSCs), leading to a disruption in the balance between osteogenic and adipogenic differentiation. Additionally, gene set enrichment analysis (GSEA) suggested that PANK2 may participate in bone metabolic regulation via chemokine signaling pathway and the neuro-osteogenic axis. This study highlights for the first time the critical role of PANK2 in PFAS-induced osteoporosis and provides novel mechanistic insights and potential therapeutic targets for the prevention and treatment of environmentally induced bone metabolic disorders.
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spelling doaj-art-28b0661c031d49609e15e99fc6e4e3b32025-08-20T04:02:31ZengElsevierEcotoxicology and Environmental Safety0147-65132025-09-0130211859310.1016/j.ecoenv.2025.118593Multi-level evidence reveals PANK2 as a potential target of PFOA/PFOS-induced bone metabolism disruption: From network toxicology to in vitro validationYiming Shao0Wenhao Fan1Department of Laboratory Medicine, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, China; Center of Stem Cell and Regenerative Medicine, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, China; Correspondence to: No.16 Tongbai North Road, Zhengzhou, China.Department of Foot and Ankle Surgery, Zhengzhou Orthopedic Hospital Affiliated to Henan University, Zhengzhou, ChinaPerfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) are two representative per- and polyfluoroalkyl substances (PFAS) that have attracted increasing attention due to their environmental persistence and potential health risks, while their bone toxicity remains unclear. In this study, we systematically investigated the toxicological mechanisms of PFOA and PFOS on bone metabolism by integrating network toxicology, molecular docking and molecular dynamics simulations, and in vitro cellular experiments. Pantothenate kinase 2 (PANK2) was identified as a key target through the intersection of multiple databases and cross-validation using three machine learning algorithms. Molecular docking and dynamics simulations demonstrated that PFOA and PFOS can stably bind to PANK2 protein. In vitro experiments further confirmed that both PFOA and PFOS significantly suppressed PANK2 expression in bone marrow mesenchymal stem cells (BMSCs), leading to a disruption in the balance between osteogenic and adipogenic differentiation. Additionally, gene set enrichment analysis (GSEA) suggested that PANK2 may participate in bone metabolic regulation via chemokine signaling pathway and the neuro-osteogenic axis. This study highlights for the first time the critical role of PANK2 in PFAS-induced osteoporosis and provides novel mechanistic insights and potential therapeutic targets for the prevention and treatment of environmentally induced bone metabolic disorders.http://www.sciencedirect.com/science/article/pii/S0147651325009388PFOAPFOSOsteoporosisPANK2Network toxicologyMolecular docking
spellingShingle Yiming Shao
Wenhao Fan
Multi-level evidence reveals PANK2 as a potential target of PFOA/PFOS-induced bone metabolism disruption: From network toxicology to in vitro validation
Ecotoxicology and Environmental Safety
PFOA
PFOS
Osteoporosis
PANK2
Network toxicology
Molecular docking
title Multi-level evidence reveals PANK2 as a potential target of PFOA/PFOS-induced bone metabolism disruption: From network toxicology to in vitro validation
title_full Multi-level evidence reveals PANK2 as a potential target of PFOA/PFOS-induced bone metabolism disruption: From network toxicology to in vitro validation
title_fullStr Multi-level evidence reveals PANK2 as a potential target of PFOA/PFOS-induced bone metabolism disruption: From network toxicology to in vitro validation
title_full_unstemmed Multi-level evidence reveals PANK2 as a potential target of PFOA/PFOS-induced bone metabolism disruption: From network toxicology to in vitro validation
title_short Multi-level evidence reveals PANK2 as a potential target of PFOA/PFOS-induced bone metabolism disruption: From network toxicology to in vitro validation
title_sort multi level evidence reveals pank2 as a potential target of pfoa pfos induced bone metabolism disruption from network toxicology to in vitro validation
topic PFOA
PFOS
Osteoporosis
PANK2
Network toxicology
Molecular docking
url http://www.sciencedirect.com/science/article/pii/S0147651325009388
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AT wenhaofan multilevelevidencerevealspank2asapotentialtargetofpfoapfosinducedbonemetabolismdisruptionfromnetworktoxicologytoinvitrovalidation