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Micro/nanoplastic-driven cardiovascular senescence and multi-target intervention by traditional Chinese medicine
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Researchers reviewed how micro- and nanoplastics accumulate in cardiovascular tissues and accelerate cellular aging through mitochondrial damage, epigenetic changes, telomere shortening, and chronic inflammation, while also highlighting traditional Chinese medicine's multi-target compounds as a potential countermeasure by simultaneously addressing oxidative stress, fibrosis, and cell death pathways.
Micro/nanoplastics (MNPs), pervasive environmental pollutants, accumulate in cardiovascular tissues and drive premature aging through multiscale pathophysiological cascades. This review synthesizes evidence establishing environmental phenotypic aging as a novel mechanistic link between MNP exposure and cardiovascular senescence. MNPs induce mitochondrial damage involving cristae disruption and mtDNA leakage activating cGAS-STING, epigenetic reprogramming encompassing METTL3-mediated m6A hypermethylation and SIRT1/3 suppression, telomere attrition, and NLRP3 inflammasome-dependent inflammaging. It is crucial to note that traditional Chinese medicine (TCM) has been identified as an effective countermeasure. The multi-compound therapeutics of TCM simultaneously target oxidative stress, inflammatory fibrosis, and cell death pathways, thereby restoring cardiovascular homeostasis. By combining environmental toxicology and geroprotection research, this work establishes TCM's holistic approach as a paradigm-shifting intervention against the cardiovascular aging caused by plastic pollution, providing practical strategies to address a mounting public health crisis.
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Nanoplastics causes heart aging/myocardial cell senescence through the Ca2+/mtDNA/cGAS-STING signaling cascade
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Researchers discovered that nanoplastics can cause heart aging by entering heart muscle cells and triggering a chain reaction: they damage mitochondria (the cell's energy source), which leaks DNA into the cell, activating an immune alarm system called the cGAS-STING pathway. This is the first study to reveal how long-term nanoplastic exposure could accelerate heart aging, raising concerns about the cardiovascular effects of plastic pollution.
Microplastics and Nanoplastics in Cardiovascular Disease: An Emerging Cardiovascular Risk Factor
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Researchers reviewed mounting experimental and early clinical evidence that microplastics and nanoplastics cross epithelial barriers, accumulate in arterial plaques, cardiac tissue, and thrombi, and trigger oxidative stress and coagulation dysregulation, framing these particles as an emerging cardiovascular risk factor that warrants integration into disease prevention frameworks.
Effects of micro- and nano-plastics exposure on cellular senescence: an overview.
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Researchers review how micro- and nanoplastics trigger cellular senescence — a state of permanent cell cycle arrest — through oxidative stress and DNA damage, activating pathways like cGAS-STING and NF-κB that elevate risk for age-related diseases, and survey potential therapeutic strategies to counter these effects.
Microplastics induce mitochondrial dysfunction and accelerate cardiovascular pathogenesis
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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.
Micro- and Nanoplastics Exposure Across the Lifespan: One Health Implications for Aging and Longevity
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Researchers reviewed evidence on micro- and nanoplastic exposure across the human lifespan through a One Health lens, finding that MNPs trigger oxidative stress, inflammation, mitochondrial dysfunction, and cellular senescence—mechanisms central to aging—and that older adults face compounded risk from lifetime accumulation and diminished physiological resilience, though direct epidemiological data in this population remain sparse.
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