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MPTmouse
Summary
Scientists exposed mice to microplastics and found that even without causing visible damage, these tiny plastic particles quietly rewired gene activity across multiple organs—especially when combined with aging. Using AI, the researchers linked these gene changes to increased vulnerability for diseases like metabolic disorders and infections, suggesting microplastics may not directly cause illness but could prime the body to be more susceptible when other health stressors hit. This mouse-based research offers early clues about hidden risks of everyday plastic exposure, though more work is needed to confirm these effects in humans.
Microplastics (MPs) exposure has emerged as a global environmental crisis with potential threats to human health, particularly concerning the development of diseases. However, under conditions that simulate real-world human exposure, significant challenges remain in elucidating the molecular mechanisms underlying MPs-induced effects and their relevance to disease pathogenesis. In this study, we developed MPTmouse, a comprehensive and quantitative map of the mouse transcriptomic regulation by MPs exposure. We observed widespread remodeling of the transcriptome and molecular interaction networks driven by MPs across multiple tissues, even in the absence of overt tissue damage. When MPs were combined with additional physiological stressors such as aging, we identified pronounced alterations in MPs-associated regulatory pathways. Furthermore, MPs exposure can induce a state of pathological vulnerability, characterized by perturbation of specific key genes, that predisposing individuals to disease progression when interacting with other factors such as metabolic disorders, infections, and aging. Using an artificial intelligence approach, we dissected the molecular basis linking MP-perturbed gene networks to major human diseases. Collectively, we present MPTmouse together with a disease association compendium as a framework for understanding the regulatory impact of MPs on physiology and aging.