Molecular mechanisms involved in atherogenic effects of Cd exposure

Molecular mechanisms involved in atherogenic effects of Cd exposure. Cd-induced ROS overproduction promotes LDL oxidation and oxLDL internalization by macrophages, resulting in foam cell formation. LDL oxidation is also aggravated by Cd-induced PON1 inhibition. Up-regulated expression of adhesion molecules including ICAM1 and VCAM1 following Cd exposure increases monocyte adhesion and infiltration, with their subsequent transformation to foam cells. Proinflammatory effect of Cd also contributes to atherogenesis through promotion of TMAO-induced NF-κB and subsequent NLRP3 inflammasome activation, as well as JAK2/STAT3-dependent M1 macrophage (Mφ) polarization. Finally, Cd-induced alterations of gut microbiota composition along with increased gut wall permeability results in an increase in circulating LPS levels, also promoting proinflammatory signaling. Different colors (pink, grey, blue, yellow) are indicative of distinct pathways for better visualization. Red and blue arrows show the increase and decrease effects

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Association between Heavy Metals, Metalloids and Metabolic Syndrome: New Insights and Approaches (2023) Airton C. Martins, et al. Toxics. 2023 Aug;11(8). Figure: F2. Homo sapiens

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