[Microplastics and thrombo-inflammation in acute ischemic stroke : adding fuel to the fire].
Source: PubMed, NCBI / U.S. National Library of Medicine
The widespread use of petroleum-derived plastics has led to massive environmental exposure to micro- and nanoplastics (MNPs), generated by the degradation of plastic polymers. Ubiquitous, these contaminants enter the body mainly through the gastrointestinal tract, but also via inhalation or iatrogenic sources, reach the systemic circulation, and accumulate in the brain. Recent data show increasing cerebral concentrations of MNPs, paralleling their environmental rise, as well as their presence in human thrombi and atherosclerotic plaques. Acute ischemic stroke, a leading cause of mortality and disability worldwide, is driven by thrombo-inflammatory mechanisms involving coordinated activation of the endothelium, platelets, and leukocytes. Converging preclinical and clinical evidence suggests that MNPs amplify these processes. They promote intestinal permeability and induce systemic and local inflammation through activation of all cellular components involved in thrombo-inflammation. In addition, MNPs may contribute to the development and destabilization of atherosclerotic plaques and, indirectly, to atrial fibrillation via activation of the thrombo-inflammatory processes. Despite methodological limitations, these findings indicate that MNPs represent an emerging environmental factor that may worsen both the risk and prognosis of acute ischemic stroke. Preventive, detection, and exposure-control strategies are therefore urgently needed to address this major public health challen
Abstract
The widespread use of petroleum-derived plastics has led to massive environmental exposure to micro- and nanoplastics (MNPs), generated by the degradation of plastic polymers. Ubiquitous, these contaminants enter the body mainly through the gastrointestinal tract, but also via inhalation or iatrogenic sources, reach the systemic circulation, and accumulate in the brain. Recent data show increasing cerebral concentrations of MNPs, paralleling their environmental rise, as well as their presence in human thrombi and atherosclerotic plaques. Acute ischemic stroke, a leading cause of mortality and disability worldwide, is driven by thrombo-inflammatory mechanisms involving coordinated activation of the endothelium, platelets, and leukocytes. Converging preclinical and clinical evidence suggests that MNPs amplify these processes. They promote intestinal permeability and induce systemic and local inflammation through activation of all cellular components involved in thrombo-inflammation. In addition, MNPs may contribute to the development and destabilization of atherosclerotic plaques and, indirectly, to atrial fibrillation via activation of the thrombo-inflammatory processes. Despite methodological limitations, these findings indicate that MNPs represent an emerging environmental factor that may worsen both the risk and prognosis of acute ischemic stroke. Preventive, detection, and exposure-control strategies are therefore urgently needed to address this major public health challenge.