Abstract
People living with hypertension have a higher risk of developing heart diseases, and hypertension remains a top cause of mortality. In hypertension, some detrimental changes occur in the arterial wall, which include physiological and biochemical changes. Furthermore, this disease is characterized by turbulent blood flow, increased fluid shear stress, remodeling of the blood vessels, and endothelial dysfunction. As a complex disease, hypertension is thought to be caused by an array of factors, its etiology consisting of both environmental and genetic factors. The Mosaic Theory of hypertension states that many factors, including genetics, environment, adaptive, neural, mechanical, and hormonal perturbations are intertwined, leading to increases in blood pressure. Long-term efforts by several investigators have provided invaluable insight into the physiological mechanisms responsible for the pathogenesis of hypertension, and these include increased activity of the sympathetic nervous system, overactivation of the renin–angiotensin–aldosterone system (RAAS), dysfunction of the vascular endothelium, impaired platelet function, thrombogenesis, vascular smooth muscle and cardiac hypertrophy, and altered angiogenesis. Exosomes are extracellular vesicles released by all cells and carry nucleic acids, proteins, lipids, and metabolites into the extracellular environment. They play a role in intercellular communication and are involved in the pathophysiology of diseases. Since the discovery of exosomes in the 1980s, numerous studies have been carried out to understand the biogenesis, composition, and function of exosomes. In this review, we will discuss the role of exosomes as intercellular messengers in hypertension.
Highlights
Despite impacting nearly 1.13 billion people worldwide [1], the pathophysiology of hypertension remains elusive
Exosomes from reverse-dipping blood pressure (RDBP) patients caused an increase in the permeability of endothelial tight junctions and adhesion molecule expression, stimulating endothelial dysfunction in human dermal microvascular endothelial cells monolayers [75]
NFκB translocates into the nucleus where it regulates the transcription of genes involved in the pathogenesis of inflammatory lesions. These genes encode cytokines such as interleukin-6 and tumor necrosis factor-α, chemokines such as monocyte chemotactic protein 1 (MCP-1), and adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and platelet endothelial cell adhesion molecule, all involved in the recruitment of monocytes/macrophages to sites of inflammation in the vascular wall [87]
Summary
Despite impacting nearly 1.13 billion people worldwide [1], the pathophysiology of hypertension remains elusive. Increased peripheral resistance is largely attributed to vascular remodeling (either inward eutrophic remodeling or hypertrophic remodeling) and endothelial dysfunction, and these modifications are consequences of an exacerbation in physiological processes such as apoptosis, inflammation, and vascular fibrosis [4,5]. In this context, exosomes become a potential source of molecules that could trigger these processes, since exosomes are released from the cells through exocytosis, and the content of exosomes can vary from cell signaling molecules to cell waste; further, exosomes can contain secretions meant to enhance the cell’s local environment [6]. The involvement of exosomes may be crucial to understanding the systemic communication of cells in hypertensive patients and can shed light on the advancement of the pathology of hypertension
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