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. Author manuscript; available in PMC: 2022 Jul 1.
Published in final edited form as: Neurochem Int. 2021 May 5;147:105054. doi: 10.1016/j.neuint.2021.105054

Figure 4. ADK mediated epigenetic mechanisms in vascular diseases.

Figure 4.

Schematic shows ADK plays an important role as an epigenetic regulator in various vascular pathologies. (i) Hypoxia induces ADK downregulation in endothelial cells, leading to hypomethylation of vascular endothelial growth factor receptor 2 (VEGFR2) and thereby promotes angiogenesis. (ii) In myeloid cells, increase in ADK expression and associated DNA methylation represses the ABCG1 gene, a key regulator of cholesterol trafficking, resulting in the formation of foam cells and atherosclerotic lesions. (iii) In endothelial cells, inflammation (TNF-α)-induced upregulation of ADK promotes histone methylation H3K4 resulting in increased expression of adhesion molecules ICAM-1 and VCAM-1. (iv) In vascular smooth muscle cells (VSMC), ADK expression was associated with DNA hypermethylation and therefore suppression of the KLF4 gene expression, an anti-proliferation gene, resulting in increased VSMC proliferation and neointima formation.