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Biological Modulation of Autophagy by Nanoplastics: A Current Overview
Summary
This review examines how nanoplastics interfere with autophagy, the cell's natural recycling and cleanup process. While cells initially activate autophagy to deal with nanoplastic particles, prolonged exposure can overwhelm this system, leading to cell damage and death. Understanding this process is important because it may explain how long-term nanoplastic exposure contributes to tissue damage and disease in humans.
Nanoplastics (NPs), an emerging class of environmental pollutants, are increasingly recognized for their potential to interfere with critical cellular processes. Autophagy, a conserved degradative pathway essential for maintaining cellular homeostasis and adaptation to stress, has recently become a focal point of nanotoxicology research. This review synthesizes current evidence on the interactions between NPs and autophagic pathways across diverse biological systems. Findings indicate that NPs can trigger autophagy as an early cellular response; however, prolonged exposure may lead to autophagic dysfunction, contributing to impaired cell viability and disrupted signaling. Particular attention is given to the physiochemical properties of NPs such as size, surface charge, and polymer type, which influence cellular uptake and intracellular trafficking. We also highlight key mechanistic pathways, including oxidative stress and mTOR modulation. Notably, most available studies focus almost exclusively on polystyrene (PS)-based NPs, with limited data on other types of polymers, and several reports lack comprehensive assessment of autophagic flux or downstream effects. In conclusion, a better understanding of NP-autophagy crosstalk-particularly beyond PS-is crucial to evaluate the real toxic potential of NPs and guide future research in human health and nanotechnology.