Table 1. Overview of potential strategies for targeting altered metabolism in atherosclerosis discussed in this review.

Therapy	Target	Experimental model	Therapeutic target/goal	Reference
miR-124 Supplementation	PTBP1 and PKM2	blood outgrowth endothelial cells from patients with pulmonary arterial hypertension	Restoring mitochondrial activity Normalizing glycolysis	[62]
Supplementation with the anti-oxidant MitoQ	Mitochondria	Aged mice	Reduction of ROS Restoring endothelium-dependent dilation	[68]
Supplementation with the anti-oxidant MitoQ	Mitochondria	healthy older adults (60–79 years)	Restoring endothelium dependent dilation	[69]
Small molecule 3PO	PFKFB3	Orthotopic pancreatic and B16-F10 melanoma tumour models	Normalization of the vasculature	[11]
Small molecule 3PO	PFKFB3	in vitro HUVEC spheroid models in vivo zebrafish embryos and postnatal mouse retinas	Reducing neovascularization	[87]
Small molecule 3PO	PFKFB3	Peripheral blood mononuclear cells	Reducing inflammation	[78]
Specific inhibitor PFK158	PFKFB3	LDLr-/- mice on a high fat diet	Increasing atherosclerotic plaque stability	[16]
Atorvastatin (40 mg/day)	eNOS activity	Patients with acute coronary syndrome	Increasing FMD, decreasing E-selectin, sICAM and CRP	[81]
AKCEA-APO(a)-LRx	apolipoprotein(a)	Phase 1 and 2 clinical trials	Lowering Lp(a), Reducing the pro-inflammatory phenotype of circulating monocytes	[88,89]
Monoclonal antibody E06	Oxidized phospholipids	Human arterial endothelial cells	Decreasing Lp(a)-induced EC inflammation and activation	[4]