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<p>Microplastics and nanoplastics (MNPs) are becoming ubiquitous environmental pollutants, with increasing evidence of their systemic toxicity. MNPs are increasingly detected in human tissues, including the cardiovascular system, and have been implicated in the pathogenesis of cardiovascular disease through mitochondrial dysfunction. This review integrates mechanistic insights into how MNPs impair mitochondrial integrity, induce oxidative stress, disrupt calcium signaling, and promote genomic instability in cardiac tissue. MNPs also exacerbate inflammation, cellular senescence, mitophagy dysfunction, and pro-atherosclerotic remodeling. Furthermore, this review examines sex-specific mitochondrial responses and developmental vulnerabilities. Understanding the molecular crosstalk between MNPs exposure and mitochondrial damage may provide a foundation for targeted interventions to mitigate environmental cardiovascular risks.</p>

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Microplastics induce mitochondrial dysfunction and accelerate cardiovascular pathogenesis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月28日

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  • Tsung-Hsien Chen,
  • I.-Tseng Chu,
  • Rei-Yeuh Chang,
  • Hsiang-Chen Wang,
  • Chi-Jung Chung,
  • Tzu-Hsien Tsai,
  • Chu-Kuang Chou

摘要

Microplastics and nanoplastics (MNPs) are becoming ubiquitous environmental pollutants, with increasing evidence of their systemic toxicity. MNPs are increasingly detected in human tissues, including the cardiovascular system, and have been implicated in the pathogenesis of cardiovascular disease through mitochondrial dysfunction. This review integrates mechanistic insights into how MNPs impair mitochondrial integrity, induce oxidative stress, disrupt calcium signaling, and promote genomic instability in cardiac tissue. MNPs also exacerbate inflammation, cellular senescence, mitophagy dysfunction, and pro-atherosclerotic remodeling. Furthermore, this review examines sex-specific mitochondrial responses and developmental vulnerabilities. Understanding the molecular crosstalk between MNPs exposure and mitochondrial damage may provide a foundation for targeted interventions to mitigate environmental cardiovascular risks.