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Microplastics induce mitochondrial dysfunction and accelerate cardiovascular pathogenesis
Summary
Researchers reviewed evidence that micro- and nanoplastics detected in human cardiovascular tissues may contribute to cardiovascular disease through mitochondrial dysfunction. The study found that these particles can impair mitochondrial integrity, induce oxidative stress, disrupt calcium signaling, and promote genomic instability, suggesting a mechanistic link between plastic particle exposure and cardiovascular pathology.
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.