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. Author manuscript; available in PMC: 2018 Nov 14.
Published in final edited form as: Circulation. 2017 Sep 21;136(20):1920–1935. doi: 10.1161/CIRCULATIONAHA.117.027589

Figure 7. Proposed model for the role of HERV-K and SAMHD1 in PAH.

Figure 7

The endogenous retrovirus HERV-K is expanded, possibly as a result of an environmental or genotoxic stress. The product, HERV-K dUTPase, and the subsequent activation of vascular, inflammatory and immune cells lead to adverse vascular remodeling and PAH.