Skip to main content
. Author manuscript; available in PMC: 2022 Aug 10.
Published in final edited form as: Circulation. 2021 Jun 11;144(6):455–470. doi: 10.1161/CIRCULATIONAHA.120.050553

Figure 8: Model of TET2’s role in limiting intimal hyperplasia through preventing VSMC apoptosis.

Figure 8:

Alloantigen-primed effector T cells infiltrate into the vessel wall and elaborate IFNу, resulting in repression of VSMC TET2. TET2 repression sensitizes VSMCs to extrinsic apoptosis, leading to pathogenic crosstalk that promotes proliferation of surviving VSMCs. This crosstalk may potentially extend to resident progenitor cells, and/or extravasated circulating recipient-derived progenitor cells. These effects lead to exacerbated intimal hyperplasia.