Multiple epidemiological studies have suggested that industrialization and progressive urbanization should be considered one of the main factors responsible for the rising of
atherosclerosis in the developing world. In this scenario, the role of trace metals in the insurgence and progression of
atherosclerosis has not been clarified yet. In this paper, the specific role of selected
trace elements (
magnesium,
zinc,
selenium,
iron,
copper,
phosphorus, and
calcium) is described by focusing on the atherosclerotic prevention and pathogenesis plaque. For each
element, the following data are reported: daily intake, serum levels, intra/extracellular distribution, major roles in physiology, main effects of high and low levels, specific roles in
atherosclerosis, possible interactions with other
trace elements, and possible influences on plaque development. For each
trace element, the correlations between its levels and clinical severity and outcome of
COVID-19 are discussed. Moreover, the role of
matrix metalloproteinases, a family of
zinc-dependent
endopeptidases, as a new medical therapeutical approach to
atherosclerosis is discussed. Data suggest that
trace element status may influence both
atherosclerosis insurgence and plaque evolution toward a stable or an unstable status. However, significant variability in the action of these traces is evident: some - including
magnesium,
zinc, and
selenium - may have a protective role, whereas others, including
iron and
copper, probably have a multi-faceted and more complex role in the pathogenesis of the
atherosclerotic plaque. Finally,
calcium and
phosphorus are implicated in the calcification of
atherosclerotic plaques and in the progression of the plaque toward
rupture and severe clinical complications. In particular, the role of
calcium is debated. Focusing on the
COVID-19 pandemia, optimized
magnesium and
zinc levels are indicated as important protective tools against a severe
clinical course of the disease, often related to the ability of SARS-CoV-2 to cause a systemic inflammatory response, able to transform a stable plaque into an unstable one, with severe clinical complications.