Dear Colleagues,
Identifying and treating the rupture-prone atherosclerotic plaque remains a challenge for reducing the burden of cardiovascular diseases (CVDs). CVDs, a major cause of mortality in humans, have a complex etiology. Multiple risk factors and pathological mechanisms contribute to this disease, including metabolic perturbations in cardiomyocytes and endothelial cells. A broad study of the pathogenetic mechanisms of the CVD onset and progression has focused on the importance of endothelial dysfunction (ED) and macrophage activation in these processes. In fact, CVDs, including atherosclerosis, are the primary cause of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM). Other established risk factors are of metabolic origin such as hypercholesterolemia or associated with significant metabolic syndrome derangements such as hypertension (1). In T2DM, energy metabolism is greatly reshaped due to a deregulation of glucose and fatty acid metabolism, and insulin resistance is recognized as an important mechanism for cardiovascular dysfunction (2, 3). Therefore, the measurement of metabolic changes might have a huge impact on the discovery of clinical and pharmacological biomarkers. To date, metabolomics profiling offers a potential tool for improving noninvasive diagnostics and risk stratification in patients affected by cardiovascular and metabolic disorders. In fact, metabolic changes in response to environmental factors or endogenous stimuli are the final effect of genomic, epigenetic, transcriptomic, and proteomic interactions and, therefore, the measurement of the metabolome integrate variations in the other omics.
Due to new advances in "omics" technologies, metabolomics and its application to cardiovascular diseases continues to evolve rapidly, making it possible to perform new comprehensive tests on metabolites that are crucial in the process of CVD. The metabolic shifts are pivotal for monocyte and macrophage function as well. Contact with atherogenic particles such as oxidized phospholipids prime to a regulatory metabolic pro-inflammatory phenotype, orchestrated via pattern-recognition receptors, nuclear receptors, and other transcription factors; therefore, metabolic changes in endothelial cells, monocytes, and macrophages may have a deep effect on the inflammatory phenotype of these cells, determining their impact on the advancement of atherosclerosis (6). As inflammation and metabolic shifts are closely entwined in both immune cells as well as endothelial cells (7), therapeutic targets aiming at altering the cellular metabolism of activated cells may hold great potential in the treatment of cardiovascular patients. However, to identify appropriate therapeutic targets that could help to design disease-modifying agents, a comprehensive analysis of the transcriptome and metabolome of atherosclerotic plaque and associated cells is needed. Furthermore, the acquisition of how metabolic shifts reflect the quiescent or inflammatory state of an atherosclerotic lesion will also be helpful to identify companion biomarkers of metabolic processes that might be useful to monitor the effect of available or experimental therapeutic targets.
Despite this, the interconnection of metabolic and inflammatory processes in rupture-prone plaques is poorly understood in humans. Moreover, this topic is written to invite research conducted to investigate the characteristic of cell metabolism related to atherosclerosis progression to implement the development of personalized approaches for their prevention and treatment. The pivotal concept is based on the relationship between cell metabolism, the regulation of immune-metabolic homeostasis, and cardiovascular disease.
Dr. Celestino Sardu
Prof. Dr. Raffaele Marfella
Collection Editors
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