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Micro- and nanoplastics-mediated immunometabolic reprogramming: a systemic nexus for chronic inflammation and multi-organ disease risk
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Researchers review how micro- and nanoplastics reprogram cellular energy metabolism by stabilizing HIF-1α and driving a Warburg-like glycolytic shift in macrophages, with lipid corona formation and gut microbiota dysbiosis further amplifying systemic inflammation — collectively linking MNP exposure to cardiovascular, metabolic, and neurodegenerative disease risk.
Drp1-mediated fission and activating the cGAS-STING pathway. Furthermore, MNP induce a pseudohypoxic state that stabilizes HIF-1a, driving a glycolytic "Warburg-like" shift that promotes pro-inflammatory macrophage polarization. These intracellular perturbations are further amplified by "lipid corona" formation and gut microbiota dysbiosis, which depletes anti-inflammatory short-chain fatty acids. Collectively, this systemic immunometabolic remodeling provides a mechanistic framework for understanding MNP-related risks for cardiovascular, metabolic, and neurodegenerative disorders. This review emphasizes the necessity of integrating immunometabolic parameters into future environmental health risk assessment frameworks.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.