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本文引用的文献

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2
Vγ6/Vδ1 + γδ T cells protect from angiotensin II effects on blood pressure and endothelial function in mice.Vγ6/Vδ1 + γδ T细胞可保护小鼠免受血管紧张素II对血压和内皮功能的影响。
J Hypertens. 2025 Jan 1;43(1):109-119. doi: 10.1097/HJH.0000000000003871. Epub 2024 Sep 7.
3
Advances in Understanding of the Role of Immune Cell Phenotypes in Hypertension and Associated Vascular Disease.免疫细胞表型在高血压及相关血管疾病中的作用的认识进展
Can J Cardiol. 2024 Dec;40(12):2321-2339. doi: 10.1016/j.cjca.2024.08.270. Epub 2024 Aug 21.
4
Role of plasmacytoid dendritic cells in vascular dysfunction in mice with renovascular hypertension.浆细胞样树突状细胞在肾血管性高血压小鼠血管功能障碍中的作用。
Heliyon. 2024 May 29;10(11):e31799. doi: 10.1016/j.heliyon.2024.e31799. eCollection 2024 Jun 15.
5
Immune Mechanisms in Hypertension.高血压的免疫机制。
Hypertension. 2024 Aug;81(8):1659-1674. doi: 10.1161/HYPERTENSIONAHA.124.21355. Epub 2024 Jun 17.
6
Sex-Dependency of T Cell-Induced Salt-Sensitive Hypertension and Kidney Damage.T 细胞诱导的盐敏感性高血压和肾脏损伤的性别依赖性。
Hypertension. 2024 Jul;81(7):1511-1523. doi: 10.1161/HYPERTENSIONAHA.123.22608. Epub 2024 May 17.
7
Regarding Immune Mechanisms Driving Hypertension in REGARDS.关于REGARDS研究中驱动高血压的免疫机制。
Hypertension. 2024 Jun;81(6):1254-1256. doi: 10.1161/HYPERTENSIONAHA.124.22973. Epub 2024 May 15.
8
CD28-expressing δ T cells are increased in perivascular adipose tissue of hypertensive mice and in subcutaneous adipose tissue of obese humans.CD28 表达的 δ T 细胞在高血压小鼠的血管周围脂肪组织和肥胖人类的皮下脂肪组织中增加。
J Hypertens. 2024 Jul 1;42(7):1256-1268. doi: 10.1097/HJH.0000000000003725. Epub 2024 Mar 26.
9
Immunomodulatory Activity of Cytokines in Hypertension: A Vascular Perspective.细胞因子在高血压中的免疫调节作用:血管视角。
Hypertension. 2024 Jul;81(7):1411-1423. doi: 10.1161/HYPERTENSIONAHA.124.21712. Epub 2024 Apr 30.
10
NETosis Drives Blood Pressure Elevation and Vascular Dysfunction in Hypertension.中性粒细胞胞外诱捕网形成导致高血压血压升高和血管功能障碍。
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免疫与高血压的最新进展:肾脏中的新细胞阻滞

Recent advances on immunity and hypertension: the new cells on the kidney block.

作者信息

Dasinger John Henry, Abais-Battad Justine M, McCrorey Marice K, Van Beusecum Justin P

机构信息

Department of Physiology, School of Medicine, Tulane University, New Orleans, Louisiana, United States.

Department of Physiology, Medical College of Georgia, August University, Augusta, Georgia, United States.

出版信息

Am J Physiol Renal Physiol. 2025 Mar 1;328(3):F301-F315. doi: 10.1152/ajprenal.00309.2024. Epub 2025 Jan 24.

DOI:10.1152/ajprenal.00309.2024
PMID:39853324
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12176069/
Abstract

Over the past 50 years, the contribution of the immune system has been identified in the development of hypertension and renal injury. Both human and experimental animal models of hypertension have demonstrated that innate and adaptive immune cells, along with their cytokines and chemokines, modulate blood pressure fluctuations and end organ renal damage. Numerous cell types of the innate immune system, specifically monocytes, macrophages, and dendritic cells, present antigenic peptides to T cells, promoting inflammation and the elevation of blood pressure. These T cells and other adaptive immune cells migrate to vascular and tubular cells of the kidney and promote end-organ fibrosis, damage, and ultimately hypertensive injury. Through the development of high-throughput screening, novel renal and immune cell subsets have been identified as possible contributors and regulators of renal injury and hypertension. In this review, we will consider classical immunological cells and their contribution to renal inflammation, and novel cell subsets, including renal stromal cells, that could potentially shed new light on renal injury and hypertension. Finally, we will discuss how interorgan inflammation contributes to the development of hypertension and hypertension-related multiorgan damage, and explore the clinical implications of the immunological components of renal injury and hypertension.

摘要

在过去50年中,免疫系统在高血压和肾损伤的发展过程中的作用已得到确认。高血压的人类和实验动物模型均已表明,先天性和适应性免疫细胞及其细胞因子和趋化因子可调节血压波动和终末器官肾损伤。先天性免疫系统的多种细胞类型,特别是单核细胞、巨噬细胞和树突状细胞,将抗原肽呈递给T细胞,促进炎症反应和血压升高。这些T细胞和其他适应性免疫细胞迁移至肾脏的血管和肾小管细胞,并促进终末器官纤维化、损伤,最终导致高血压性损伤。通过高通量筛选技术的发展,已鉴定出新型肾细胞和免疫细胞亚群可能是肾损伤和高血压的促成因素及调节因子。在本综述中,我们将探讨经典免疫细胞及其对肾炎症的作用,以及新型细胞亚群,包括肾基质细胞,它们可能为肾损伤和高血压带来新的见解。最后,我们将讨论器官间炎症如何导致高血压及高血压相关多器官损伤的发展,并探讨肾损伤和高血压免疫成分的临床意义。