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. Author manuscript; available in PMC: 2021 Nov 1.
Published in final edited form as: Semin Nephrol. 2020 Nov;40(6):574–585. doi: 10.1016/j.semnephrol.2020.12.004

Figure 3. Potential Mechanisms for Uric acid Involvement in Atherosclerosis, Vascular Calcification, and Cardiovascular Disease.

Figure 3.

Uric acid may be generated in endothelial cells, causing local vascular smooth muscle cell proliferation and migration via the release of PDGF, and inflammation by the release of MCP-1, with facilitation of oxidation of LDL. Urate may then be deposited in plaque, in which crystals may act as a nidus for calcium deposition and vascular calcification potentially resulting in accelerated atherosclerosis. Urate deposits may also serve as a nidus for local intravascular inflammation that may stimulate atherogenesis and/or lead to adjacent inflammatory plaque