From Environment to Endothelium: The Role of Microplastics in Vascular Aging

Microplastics, synthetic polymer particles measuring less than 5 mm, have become a widespread environmental pollutant, raising concerns over their possible effects on human health. Growing evidence links MPs to vascular aging and cardiovascular disease beyond their ecological toxicity. Upon inhalation, ingestion, or skin contact, microplastics can traverse biological barriers, circulate systemically, and accumulate in vascular tissues. Experimental investigations indicate that MPs, especially polystyrene and polyethylene in nano- and micro-sized forms, induce oxidative stress, mitochondrial dysfunction, and chronic inflammation. These disruptions activate redox-sensitive signaling pathways, such as NF-κB and NLRP3 inflammasome, causing endothelial dysfunction, vascular smooth muscle modulation, and foam cell production, indicating early vascular aging. Animal models and in vitro studies have consistently shown endothelial activation, increased cytokine production, and changes in vascular tone after exposure to MPs. Initial human research has detected microplastics in blood, thrombi, and atherosclerotic plaques, which correlate with negative cardiovascular outcomes and systemic inflammation. Notably, recent research suggests that the gut microbiota and antioxidant systems may play a role in adaptive reactions, although these processes are still not fully understood. MP-induced vascular toxicity is covered in this interdisciplinary review, highlighting molecular pathways, experimental data, and translational gaps.