ArticleToxicology and applied pharmacology2024
The long-chain polyfluorinated alkyl substance perfluorohexane sulfonate (PFHxS) promotes bone marrow adipogenesis.
Article in Toxicology and applied pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Article
- The osteoporotic niche as a metabolic sanctuary for breast cancer dormancy and reactivation: A mechanistic perspective.iScience · 2026Review
- Sorbent Intervention to Reduce Per- and Polyfluoroalkyl Substances (PFAS) in Maternal Reproductive Tissues and Transgenerational Translocation in Sprague-Dawley Rats.Journal of hazardous materials advances · 2026Article
- Per- and polyfluoroalkyl substances and adolescent bone mineral density: assessing periods of susceptibility.Journal of the Endocrine Society · 2026Article
- Per- and polyfluorinated substances (PFAS) promote osteoclastogenesis and bone loss through PPARα activation.Toxicology reports · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Per- and polyfluoroalkyl substances (PFAS) bioaccumulate in different organ systems, including bone. While existing research highlights the adverse impact of PFAS on bone density, a critical gap remains in understanding the specific effects on the bone marrow microenvironment, especially the bone marrow adipose tissue (BMAT). Changes in BMAT have been linked to various health consequences, such as the development of osteoporosis and the progression of metastatic tumors in bone. Studies presented herein demonstrate that exposure to a mixture of five environmentally relevant PFAS compounds promotes marrow adipogenesis in vitro and in vivo. We show that among the components of the mixture, PFHxS, an alternative to PFOS, has the highest propensity to accumulate in bone and effectively promote marrow adipogenesis. Utilizing RNAseq approaches, we identified the peroxisome proliferator-activated receptor (PPAR) signaling as a top pathway modulated by PFHxS exposure. Furthermore, we provide results suggesting the activation and involvement of PPAR-gamma (PPARγ) in PFHxS-mediated bone marrow adipogenesis, especially in combination with high-fat diet. In conclusion, our findings demonstrate the potential impact of elevated PFHxS levels, particularly in occupational settings, on bone health, and specifically bone marrow adiposity. This study contributes new insights into the health risks of PFHxS exposure, urging further research on the relationship between environmental factors, diet, and adipose tissue dynamics.
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