Cardiac and Vascular Microenvironment: Biological and Clinical Implications in Cardiology
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2018, Vol 7, Issue 4
Abstract
In the last years, the world of cardiology has turned the lights on the role of pro-inflammatory constellation of cytokines and interleukins in the pathophysiology of myocardial and vascular damage. Cardiomyocytes and vascular endothelial cells produce continuously several growth factors and small molecules, acting both in autocrine and paracrine manner, regulating their mitochondrial metabolism, the balance of intracellular calcium and also the resistance to chemotherapeutic damage. This review place same biological and biochemical basis on the involvement of the cardiac and vascular mirco environment on the cardiovascular diseases and on the cardiotoxicity related to anticancer drug exposure, with particular reference to Interleukin 1, 6, 8, Advanced Glycation End Products and lipid peroxidation. Moreover, some biological and clinical considerations will be discussed aimed to improve the cardiac and vascular microenvironment, also by using phytotherapics and anti-inflammatory drugs of synthetic or natural origin. Tissue and cellular microenvironment is a complex of interations between small molecules like interleukins, cytokines, chemokines, SIRNA, hormones acting in autocrine and paracrine manner in cardiomyocytes [1]. The cardiac tissue is a pluricellular organ composed of cardiomyocytes, fibroblasts, endothelial cells, smooth muscle cells, neurons and immune cells regulating the homeostasis of the matrix deposition, neo-vascularization, inflammation and mithocondrial metabolism [2]. In the field of oncology, several work focalize their attention on the role of cancer microenvornment in the drug resistance mechanisms, growth and survival [3,4]. Inflammatory cytokines are a small category of proteins involved in several heart diseases due to their negative inotropic effects and deleterious effects on left ventricular remodeling [5]. Interleukin-1 (IL-1) is one of the main cytokine involved in the pathogenesis of coronary atherosclerosis and congestive heart failure [6]. From a biological point of view, as shown in (Figure 1), Interleukin 1, 6 and 8 via their receptors, activates inflammation pathways of crucial interest in cardiology, including NfkB , the type I myeloid differentiation factor (MyD88) and criopyrin. MyD88 and cripririne work in synergism leading to the activation of inflammation increasing the gene expression and transcription of other pro-inflammatory, atherogenic and cardiotoxic interleukins like Interleukin 8 and 6. Interleukin 6 is a cytokine able to bind two type of receptors (soluble or membranarian receptor) stimulating the high sensitivity C‐reactive protein HS-CRP) and fibrinogen hepatic synthesis promoting tissue inflammation and atherosclerosis processes [7]. Clinically, men with high plasma IL‐6 have an increased risk of myocardial infarction [8]. However, activated cryopyrin, derived from IL-1 pathways in cardiomiocytes, stimulate the synthesis of Caspase 1 therefore promoting apoptosis with increased risk of myocardial infarction. Furthermore, Interleukin 1 leads to the activation of another protein called p38-MAPK which, in cardiomyocyte, increases the synthesis of nitric oxide which decreases the synthesis of cellular energy, called ATP, and disregulate calcium metabolism in the sarcoplasmic reticulum of the cardiomyocyte. Dysregulation of the intracellular calcium induced by the IL1 - p38MAPK axis dysregulate the contractility of the cardiomyocyte which is also exacerbated by the inhibitory action of the cryopyrin on the phospholamban (one of the regulators of the calcium influx in cardiomyocytes). The multiple regulation of cardiac metabolism from interleukins and their receptors become a point of attention in the field of cardiology and cardioncology.
Authors and Affiliations
Quagliariello V, Piscopo G, Maurea N
Keywords
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- EP ID EP592907
- DOI 10.26717/BJSTR.2018.07.001523
- Views 190
- Downloads 0
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