Inflammation and oxidative stress in salt sensitive hypertension; The role of the NLRP3 inflammasome.
Autor: | Ertuglu LA; Division of Nephrology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, United Staes., Mutchler AP; Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, United States., Yu J; Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, United States., Kirabo A; Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, United States. |
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Jazyk: | angličtina |
Zdroj: | Frontiers in physiology [Front Physiol] 2022 Dec 22; Vol. 13, pp. 1096296. Date of Electronic Publication: 2022 Dec 22 (Print Publication: 2022). |
DOI: | 10.3389/fphys.2022.1096296 |
Abstrakt: | Salt-sensitivity of blood pressure is an independent risk factor for cardiovascular disease and affects approximately half of the hypertensive population. While the precise mechanisms of salt-sensitivity remain unclear, recent findings on body sodium homeostasis and salt-induced immune cell activation provide new insights into the relationship between high salt intake, inflammation, and hypertension. The immune system, specifically antigen-presenting cells (APCs) and T cells, are directly implicated in salt-induced renal and vascular injury and hypertension. Emerging evidence suggests that oxidative stress and activation of the NLRP3 inflammasome drive high sodium-mediated activation of APCs and T cells and contribute to the development of renal and vascular inflammation and hypertension. In this review, we summarize the recent insights into our understanding of the mechanisms of salt-sensitive hypertension and discuss the role of inflammasome activation as a potential therapeutic target. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2022 Ertuglu, Mutchler, Yu and Kirabo.) |
Databáze: | MEDLINE |
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