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. 2021 Oct 23;12(11):992. doi: 10.1038/s41419-021-04283-6

Fig. 6. Schematic cartoon showing the mechanism of soluble epoxide hydrolase (sEH)-related vascular calcification.

Fig. 6

Under chronic kidney disease (CKD) condition, sEH interacted with Sirtuin 3 (Sirt3), leading to Sirt3 instable and degradation. This relative Sirt3 downregulation induced the increased acetylation of peroxisome proliferator-activated receptor γ co-activator-1 alpha (PGC-1α). Acetylated PGC-1α could not exert its function on gene transcription. Furthermore, the mitochondrial adenosine triphosphate (ATP) production and morphology were also impaired. All these changes triggered vascular smooth muscle cell (VSMC) phenotypic transition and calcium deposition. When sEH deletion, the sEH–Sirt3 complex could not be created and Sirt3 turned to be more stable. The sustained level of Sirt3 was able to increase the function of PGC-1α and ameliorate the mitochondrial dysfunction. As a result, VSMC phenotypic transition and calcium deposition were reduced, and vascular calcification was inhibited. TF transcription factor.