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. Author manuscript; available in PMC: 2021 Jun 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2020 Apr 16;40(6):e153–e165. doi: 10.1161/ATVBAHA.120.314360

Figure 6. Proposed mechanism for macrophage-associated calcification in Notch1+/− calcific aortic valve disease.

Figure 6.

Notch1+/− aortic valve interstitial cells (AVICs) secrete pro-inflammatory factors (A) leading to increased macrophage infiltration and maturation to a proinflammatory phenotype (B). These infiltrating macrophages alter STAT3 splice products to decrease STAT3β (C). Decrease of STAT3β removes inhibition of STAT3α and RUNX2 (D), promoting cellular stiffening and expression of osteogenic transcripts, respectively, and leading to valvular calcification (E).