Abstract
Cellular metabolism has been known for its role in bioenergetics. In recent years, much light has been shed on the reprogrammable cellular metabolism underlying many vital cellular processes, such as cell activation, proliferation, and differentiation. Metabolic reprogramming in immune and endothelial cells (ECs) is being studied extensively. These cell compartments are implicated in inflammation and pathogenesis of many diseases but their similarities in metabolic reprogramming have not been analyzed in detail. One of the most notable metabolic reprogramming is the Warburg-like effect, famously described as one of the hallmarks of cancer cells. Immune cells and ECs can display this phenotype that is characterized by a metabolic switch favoring glycolysis over oxidative phosphorylation (OXPHOS) in aerobic conditions. Though energy-inefficient, aerobic glycolysis confers many benefits to the respiring cells ranging from higher rate of adenosine triphosphate production to maintaining redox homeostasis. Chemical and biological regulators either promote or perturb this effect. In this review, nitric oxide, hypoxia-inducible factor, and adenosine monophosphate-activated protein kinase have been discussed for their common involvement in metabolic reprogramming of both systems. From in vitro and animal studies, various discrepancies exist regarding the effects of those regulators on metabolic switch. However, it is generally accepted that glycolysis favors inflammatory reactions while OXPHOS favors anti-inflammatory processes. The reasons for such observation are currently subject of intense studies and not completely understood. Finally, metabolic reprogramming in immune cells and ECs does not limit to the physiological state in health but can also be observed in pathological states, such as atherosclerosis and cancer. These new insights provide us with a better understanding of the similarities in metabolic reprogramming across a number of cell types, which could pave the way for future research and possible metabolic-based therapeutics.
Highlights
Cellular metabolism has been sidelined for many years and it was only seen as the series of sequential pathways involved in converting fuel sources, such as glucose, fatty acids, ketones, and amino acids to generate packets of cellular energy in the form of adenosine triphosphate (ATP)
The demand for an expensive amount of energy from metabolically active processes can be met by aerobic glycolysis, which is a faster bioenergetic pathway as compared to oxidative phosphorylation (OXPHOS), granted that there is a steady stream of glucose supply [46]
Despite not many studies support a role for nitric oxide (NO)-mediated effects via rewiring of endothelial cells (ECs) metabolism, NO produced from endothelial nitric oxide synthase (eNOS) is theoretically capable of interacting with the immune system and, it represents a topic of interest for further investigation
Summary
Reviewed by: Alf Hamann, Deutsches RheumaForschungszentrum (DRFZ), Germany Bin Li, Shanghai Jiao Tong University School of Medicine, China Matthias Lochner, Center for Experimental and Clinical Infection Research, Germany. Metabolic reprogramming in immune and endothelial cells (ECs) is being studied extensively. It is generally accepted that glycolysis favors inflammatory reactions while OXPHOS favors anti-inflammatory processes The reasons for such observation are currently subject of intense studies and not completely understood. Metabolic reprogramming in immune cells and ECs does not limit to the physiological state in health but can be observed in pathological states, such as atherosclerosis and cancer. These new insights provide us with a better understanding of the similarities in metabolic reprogramming across a number of cell types, which could pave the way for future research and possible metabolic-based therapeutics
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