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<p>The ubiquity of per- and polyfluoroalkyl substances (PFASs) such as perfluorooctanoic acid (PFOA) in environment at considerable concentrations arouses great concern over their ecotoxicological risks. Although normal cardiac function is crucial for the health and even survival of an animal, the cardiotoxicity of PFASs has never been evaluated in marine invertebrates. Taking PFOA and the thick-shell mussel as representatives, the effects of a 28-day exposure to PFOA (at levels of 0.5 and 5&#xa0;μg/L) on cardiac performance and potential underlying&#xa0;mechanisms were assessed in this study. Results demonstrated that PFOA-exposed mussels exhibited significant lower heart rate as well as product of heart rate and pulse wave amplitude, but markedly higher coefficient of variation for the interpulse duration, indicating an evident cardiac performance disruption by PFOA. Meanwhile, both structural (indicated by higher levels of fibrosis and transcriptomic/metabolomic evidence suggestive of cardiomyocyte hypertrophy) and metabolic cardiac remodeling (evidenced by lower level of ATP and disruption of metabolism-related pathways) were observed in PFOA-exposed mussels. Moreover, histological examination, biochemical assays, as well as comparative transcriptomic and metabolomic analyses illustrated that exposure of mussels to PFOA resulted in notably aggravated inflammation, apoptosis, oxidative stress, and energy deficiency. Collectively, these findings illustrated that PFOA may disrupt cardiac performance of the thick-shell mussel by triggering adverse cardiac remodeling, the far-reaching impacts of which warrant more attention.</p>

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Perfluorooctanoic acid (PFOA) disrupts cardiac performance of the thick-shell mussel Mytilus coruscus by triggering structural and metabolic cardiac remodeling

  • 期刊论文

  • 发表日期：

    2026年4月14日

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  • Yingying Yu,
  • Kuankuan Yuan,
  • Conghui Shan,
  • Difei Tong,
  • Weixia Zhang,
  • Wei Shi,
  • Haibin Yu,
  • Guangxu Liu

摘要

The ubiquity of per- and polyfluoroalkyl substances (PFASs) such as perfluorooctanoic acid (PFOA) in environment at considerable concentrations arouses great concern over their ecotoxicological risks. Although normal cardiac function is crucial for the health and even survival of an animal, the cardiotoxicity of PFASs has never been evaluated in marine invertebrates. Taking PFOA and the thick-shell mussel as representatives, the effects of a 28-day exposure to PFOA (at levels of 0.5 and 5 μg/L) on cardiac performance and potential underlying mechanisms were assessed in this study. Results demonstrated that PFOA-exposed mussels exhibited significant lower heart rate as well as product of heart rate and pulse wave amplitude, but markedly higher coefficient of variation for the interpulse duration, indicating an evident cardiac performance disruption by PFOA. Meanwhile, both structural (indicated by higher levels of fibrosis and transcriptomic/metabolomic evidence suggestive of cardiomyocyte hypertrophy) and metabolic cardiac remodeling (evidenced by lower level of ATP and disruption of metabolism-related pathways) were observed in PFOA-exposed mussels. Moreover, histological examination, biochemical assays, as well as comparative transcriptomic and metabolomic analyses illustrated that exposure of mussels to PFOA resulted in notably aggravated inflammation, apoptosis, oxidative stress, and energy deficiency. Collectively, these findings illustrated that PFOA may disrupt cardiac performance of the thick-shell mussel by triggering adverse cardiac remodeling, the far-reaching impacts of which warrant more attention.