Elisa Persiani

Plastic use dramatically increased over the past few years. Besides obvious benefits, the consequent plastic waste and mismanagement in disposal have caused ecological problems. Plastic abandoned in the environment is prone to segregation, leading to the generation of microplastics (MPs) and nanoplastics (NPs), which can reach aquatic and terrestrial organisms. MPs/NPs in water can access fish’s bodies through the gills, triggering an inflammatory response in loco. Furthermore, from the gills, plastic fragments can be transported within the circulatory system altering blood biochemical parameters and hormone levels and leading to compromised immunocompetence and angiogenesis. In addition, it was also possible to observe an unbalanced ROS production, damage in vascular structure, and enhanced thrombosis. MPs/NPs led to cardiotoxicity, pericardial oedema, and impaired heart rate in fish cardiac tissue. MPs/NPs effects on aquatic organisms pose serious health hazards and ecological consequences because they constitute the food chain for humans. Once present in the mammalian body, plastic particles can interact with circulating cells, eliciting an inflammatory response, with genotoxicity and cytotoxicity of immune cells, enhanced haemolysis, and endothelium adhesion. The interaction of MPs/NPs with plasma proteins allows their transport to distant organs, including the heart. As a consequence of plastic fragment internalisation into cardiomyocytes, oxidative stress was increased, and metabolic parameters were altered. In this scenario, myocardial damage, fibrosis and impaired electrophysiological values were observed. In summary, MPs/NPs are an environmental stressor for cardiac function in living organisms, and a risk assessment of their influence on the cardiovascular system certainly merits further analysis.

Vascular calcification is a systemic disease contributing to cardiovascular morbidity and mortality. The pathophysiology of vascular calcification involves calcium salt deposition by vascular smooth muscle cells that exhibit an osteoblast-like phenotype. Multiple conditions drive the phenotypic switch and calcium deposition in the vascular wall; however, the exact molecular mechanisms and the connection between vascular smooth muscle cells and other cell types are not fully elucidated. In this hazy landscape, effective treatment options are lacking. Due to the pathophysiological complexity, several research models are available to evaluate different aspects of the calcification process. This review gives an overview of the in vitro cell models used so far to study the molecular processes underlying vascular calcification. In addition, relevant natural and synthetic compounds that exerted anticalcifying properties in in vitro systems are discussed.