Is the ME hypothesis "the metabolic trap" able to explain endothelial dysfunction?

Vascular endothelial dysfunction has been measured in ME patients (1).

The ME hypothesis "the metabolic trap" tell us, that the first step in the kynurenine pathway is dysregulated (2).

Dysregulated kynurenine pathway is highly associated with endothelial dysfunction and has been correlated with several cardiovascular diseases (3).

Research indicates, that IDO can be nitrated and inactivated by peroxynitrite, and that nitration of IDO-Tyr15 is the most important factor for IDO inactivation (3).

Research in apolipoprotein E knock-out mice on a high fat diet has shown: Systemic IDO inhibition by 1-methyl tryptophan (1-MT) enhances vascular inflammation with upregulation of vascular cell adhesion molecule-1 (VCAM-1) and monocyte chemoattractant protein-1 (MCP-1/CCL2), and increasing CD68+ macrophage infiltration in vascular area. Moreover, IDO inhibition-induced acceleration of atherosclerosis and vascular inflammation can be reversed by exogenous administration of the Trp catabolite 3-hydroxyanthranilic acid (3-HAA ) (3).

References:

1) Mewton et al: Large and small artery endothelial dysfunction in chronic fatigue syndrome International Journal of Cardiology, 2012 Feb 9; 154(3):335–6
ME Research UK has described the study here: Large and small artery endothelial dysfunction in chronic fatigue syndrome

2) Metabolic Traps in ME/CFS - Research Update by Dr. Robert Phair https://www.youtube.com/watch?v=Quh-77gvw4Q

3) Song et al: Abnormal kynurenine pathway of tryptophan catabolism in cardiovascular diseases Cell Mol Life Sci. 2017 Aug;74(16):2899-2916. doi: 10.1007/s00018-017-2504-2. Epub 2017 Mar 17.  https://www.ncbi.nlm.nih.gov/pubmed/28314892