Mutchler Ashley L, Haynes Alexandria Porcia, Saleem Mohammad, Jamison Sydney, Khan Mohd Mabood, Ertuglu Lale, Kirabo Annet
Department of Biomedical Sciences, Meharry Medical College, Nashville TN (A.L.M).
Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN (A.P.H., M.S., M.M.K., A.K.).
Circ Res. 2025 Jan 17;136(2):232-254. doi: 10.1161/CIRCRESAHA.124.325439. Epub 2025 Jan 16.
Access to excess dietary sodium has heightened the risk of cardiovascular diseases, particularly affecting individuals with salt sensitivity of blood pressure. Our research indicates that innate antigen-presenting immune cells contribute to rapid blood pressure increases in response to excess sodium intake. Emerging evidence suggests that epigenetic reprogramming, with subsequent transcriptional and metabolic changes, of innate immune cells allows these cells to have a sustained response to repetitive stimuli. Epigenetic mechanisms also steer T-cell differentiation in response to innate immune signaling. Immune cells respond to environmental and nutritional cues, such as salt, promoting epigenetic regulation changes. This article aims to identify and discuss the role of epigenetic mechanisms in the immune system contributing to salt-sensitive hypertension.
摄入过量膳食钠会增加心血管疾病的风险,尤其会影响血压对盐敏感的个体。我们的研究表明,先天性抗原呈递免疫细胞会导致过量钠摄入后血压迅速升高。新出现的证据表明,先天性免疫细胞的表观遗传重编程以及随后的转录和代谢变化,使这些细胞能够对重复性刺激产生持续反应。表观遗传机制还会引导T细胞在先天性免疫信号作用下发生分化。免疫细胞会对环境和营养信号(如盐)作出反应,从而促进表观遗传调控的变化。本文旨在识别和讨论表观遗传机制在导致盐敏感性高血压的免疫系统中的作用。