文献类型：期刊文献

英文题名：The multifaceted impact of a high-salt environment on the immune system and its contribution to salt-sensitive hypertension

作者：Wang, Li[1];Hu, Jihong[1,2,3];Ren, Kailun[1]

第一作者：王力;王莉;王丽

通信作者：Hu, JH[1]

机构：[1]Gansu Univ Chinese Med, Publ Hlth Sch, Lanzhou 730000, Peoples R China;[2]Gansu Univ Chinese Med, Teaching Expt & Training Ctr, Lanzhou 730000, Peoples R China;[3]Gansu Univ Chinese Med, Key Lab Dunhuang Med, Minist Educ, Lanzhou 730000, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Publ Hlth Sch, Lanzhou 730000, Peoples R China.|[10735]甘肃中医药大学;

年份：2025

卷号：44

外文期刊名：BIOCHEMISTRY AND BIOPHYSICS REPORTS

收录：Scopus(收录号：2-s2.0-105015299254);WOS:【ESCI(收录号:WOS:001569461500001)】；

基金：The work was funded by the National Natural Science Foundation of China (No. 81960614) ; Key Research and Development Program of International Science and Technology Cooperation in Gansu Province (No. 20YF3WA020) ; General project of Gansu Provincial Joint Scientific Research Fund (No. 24JRRA880) ; Experimental teaching platform of the Teaching Laboratory Centre (230516110201) .

语种：英文

外文关键词：Salt-sensitive blood pressure; MAPK; NF-kappa B; JAK/STAT; NLRP3

摘要：Salt-sensitive hypertension (SSBP) is a common form of hypertension which responds strongly to dietary sodium intake. It is also associated with a significantly higher risk of cardiovascular events and target organ damage. Traditional research has focused on how the vascular, renal and neuroendocrine systems regulate SSBP. However, this study explores the profound effects of a high-salt environment on the immune system and its central role in SSBP pathogenesis, revealing key innovative findings in this field. High salt intake activates multiple key signalling pathways (NF-kappa B, JAK/STAT, MAPK and the NLRP3 inflammasome) in immune cells, such as antigenpresenting cells, macrophages and Th17 cells, triggering significant oxidative stress and inflammatory cascades. Specific mechanisms include high salt inducing immune cells to perceive sodium ions through the ENaC channel and NCX1, activating the SGK1/FOXO1 axis and NFAT5 to drive Th17/Treg imbalance and the release of proinflammatory factors such as IL-6, IL-17A, TNF-alpha and IL-1(3.), excessive ROS production and the resulting protein modifications create new antigens (e.g. IsoLG), and gut microbiota dysbiosis (e.g. reduced Lactobacillus and elevated TMAO) amplifies systemic inflammation by reducing short-chain fatty acids (SCFAs) and increasing endotoxin release, thereby activating TLR4/NF-kappa B and other pathways. This study emphasises the novel mechanisms by which these signalling pathways NF-kappa B as the core hub of inflammation; JAK2 in CD11c+ APC cells; and p38 MAPK in endothelial dysfunction and their interactions drive SSBP. These inflammatory processes impair vascular endothelial function, affect renal sodium excretion and promote renal fibrosis. They also form a vicious cycle with sympathetic nervous system activation, which collectively drives the onset and progression of SSBP. Understanding these immune-mediated inflammatory mechanisms provides an important theoretical basis for developing novel anti-inflammatory therapeutic strategies for SSBP, such as targeting specific signalling pathways or regulating intestinal microbiota.