Immunoinflammatory and Oxidative Mechanisms in Essential Hypertension as a Chronic Subclinical Inflammation
The relevance of this work is determined by the extremely high prevalence of essential hypertension and its contribution to cardiovascular mortality, disability, and economic burden. Despite the widespread use of agents targeting the renin–angiotensin–aldosterone system, the sympathetic nervous system, and water–salt balance, uncontrolled or resistant elevation of blood pressure persists in a substantial proportion of patients, along with progressive target organ damage. This indicates the limitations of classical neurohumoral concepts and necessitates the search for new pathogenetic targets, particularly in the context of increasing comorbidity (obesity, metabolic syndrome, and gut microbiota dysbiosis). This work aimed to analyze essential hypertension as a chronic low-grade inflammation and to demonstrate that immunoinflammatory mechanisms underlie persistent hypertension and target organ remodeling. The scientific novelty of this work lies in a comprehensive consideration of the role of innate and adaptive immunity (macrophages, dendritic cells, the NLRP3 inflammasome, and T-lymphocyte subpopulations, including Th17, CD8+, and regulatory T cells [Treg]) in close association with oxidative stress, endothelial dysfunction, and activation of the renin–angiotensin–aldosterone system. The critical role of visceral obesity and gut microbiota dysbiosis as key sources of systemic low-grade inflammation that convert mechanical and metabolic stress into a sustained immune response is emphasized. Particular attention is given to the concept of inflammatory remodeling of the vascular wall, myocardium, and renal tissue as the pathogenetic basis of increased vascular stiffness, sustained hypertension, and progressive target organ damage. The practical relevance of the review lies in substantiating the prospects of immunomodulatory therapies: blockade of specific cytokine pathways, regulation of NLRP3 inflammasome activity, correction of Th17/Treg imbalance, and modulation of the gut microbiota. It is shown that the transition from an exclusively neurohumoral to an inflammatory paradigm of hypertension opens opportunities for new strategies for the prevention, early diagnosis, and treatment focused on preventing long-term inflammatory damage to target organs.
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