Micro- and nanoplastics (MNPs) enter the human body through oral ingestion, inhalation, and dermal absorption, and accumulating evidence links this ubiquitous exposure to accelerated aging and age-related pathologies including cardiovascular and neurodegenerative disease. This review maps the mechanistic chain: MNPs disrupt gut microbiome composition, which in turn amplifies oxidative stress, chronic low-grade inflammation, cellular senescence, and mitochondrial dysfunction, while also distorting epigenetic regulation. The central signaling culprit identified is the TLR4/NF-κB inflammatory pathway — a well-established driver of inflammaging.
As a review rather than original experimental research, this paper synthesizes existing literature rather than generating new causal data — an important caveat. That said, the framing of an "MNPs-gut microbiome aging axis" represents meaningful conceptual consolidation. The TLR4/NF-κB connection is biologically credible: microplastics act as persistent irritants that could chronically prime innate immune signaling, mirroring mechanisms seen with endotoxins and other gut-derived inflammatory triggers. What's underexplored in the field — and likely here — is dose-response clarity: humans vary enormously in MNP exposure and microbiome resilience. The proposed multi-pronged interventions (dietary, probiotic, environmental) are directionally sound but remain speculative without randomized trial data. For health-conscious adults, this reinforces reducing plastic food contact, prioritizing microbiome diversity, and monitoring the rapidly growing body of MNP-specific intervention research. Incremental but timely synthesis.