Gamut of glycolytic enzymes in vascular smooth muscle cell proliferation: Implications for vascular proliferative diseases

Vascular smooth muscle cells (VSMCs) are the predominant cell type in the media of the blood vessels and are responsible for maintaining vascular tone. Emerging evidence confirms that VSMCs possess high plasticity. During vascular injury, VSMCs switch from a “contractile” phenotype to an extremely proliferative “synthetic” phenotype. The balance between both strongly affects the progression of vascular remodeling in many cardiovascular pathologies such as restenosis, atherosclerosis and aortic aneurism. Proliferating cells demand high energy requirements and to meet this necessity, alteration in cellular bioenergetics seems to be essential. Glycolysis, fatty acid metabolism, and amino acid metabolism act as a fuel for VSMC proliferation. Metabolic reprogramming of VSMCs is dynamically variable that involves multiple mechanisms and encompasses the coordination of various signaling molecules, proteins, and enzymes. Here, we systemically reviewed the metabolic changes together with the possible treatments that are still under investigation underlying VSMC plasticity which provides a promising direction for the treatment of diseases associated with VSMC proliferation. A better understanding of the interaction between metabolism with associated signaling may uncover additional targets for better therapeutic strategies in vascular disorders. •The molecular mechanisms underpinning metabolic reprogramming in VSMCs contribute to different VSMC phenotypes.•Targeting glycolytic flux, amino acid and fatty acid metabolism could be effective in vascular proliferative disorders.•Understanding VSMC metabolism with associated signalling may provide better therapeutic strategies in vascular disorders.