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Review
. 2022 Dec 22:13:1096296.
doi: 10.3389/fphys.2022.1096296. eCollection 2022.

Inflammation and oxidative stress in salt sensitive hypertension; The role of the NLRP3 inflammasome

Affiliations
Review

Inflammation and oxidative stress in salt sensitive hypertension; The role of the NLRP3 inflammasome

Lale A Ertuglu et al. Front Physiol. .

Abstract

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.

Keywords: hypertension; immunity; inflammasome; inflammation; salt sensitivity.

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Conflict of interest statement

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.

Figures

FIGURE 1
FIGURE 1
The proposed relationship between high sodium intake, inflammation, and salt sensitive hypertension.
FIGURE 2
FIGURE 2
The mechanism of ENaC and IsoLG-dependent NLRP3 inflammasome activation in APCs.

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References

    1. Abais J. M., Xia M., Li G., Gehr T. W., Boini K. M., Li P. L. (2014). Contribution of endogenously produced reactive oxygen species to the activation of podocyte NLRP3 inflammasomes in hyperhomocysteinemia. Free Radic. Biol. Med. 67, 211–220. 10.1016/j.freeradbiomed.2013.10.009 - DOI - PMC - PubMed
    1. Al-Solaiman Y., Jesri A., Zhao Y., Morrow J. D., Egan B. M. (2009). Low-Sodium DASH reduces oxidative stress and improves vascular function in salt-sensitive humans. J. Hum. Hypertens. 23, 826–835. 10.1038/jhh.2009.32 - DOI - PMC - PubMed
    1. Babcock M. C., Robinson A. T., Migdal K. U., Watso J. C., Wenner M. M., Stocker S. D., et al. (2019). Reducing dietary sodium to 1000 mg per day reduces neurovascular transduction without stimulating sympathetic outflow. Hypertension 73, 587–593. (Dallas, Tex: 1979). 10.1161/HYPERTENSIONAHA.118.12074 - DOI - PMC - PubMed
    1. Banoth B., Cassel S. L. (2018). Mitochondria in innate immune signaling. Transl. Res. 202, 52–68. 10.1016/j.trsl.2018.07.014 - DOI - PMC - PubMed
    1. Baradaran A., Nasri H., Rafieian-Kopaei M. (2014). Oxidative stress and hypertension: Possibility of hypertension therapy with antioxidants. J. Res. Med. Sci. 19, 358–367. - PMC - PubMed