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. 2020 Jan 10;11(1):22. doi: 10.1038/s41419-019-2215-8

Fig. 7. Proposed working schematic of PARP-1 depletion-mediated attenuation of atherosclerotic calcification in diabetes.

Fig. 7

Diabetes activates Runx2 expression and induces the osteogenic differentiation of both VSMCs and macrophages. Concurrently, diabetes promotes phenotype switching of VSMCs from the contractile phenotype to a dedifferentiated synthetic phenotype, and of macrophages to a proinflammatory M1 phenotype, which in turn aggravates VSMC calcification. PARP-1 acts on Stat1 transcription, which functions as a regulator of Runx2 expression and osteogenic differentiation. PARP-1 depletion reversed the hyperglycemia-induced synthetic phenotype switching of VSMCs and macrophage polarization by targeting Stat1. As a result, PARP-1 depletion suppresses diabetic atherosclerotic calcification.