Innate Immune Mechanisms of Arterial Hypertension and Autoimmune Disease

Jung, Rebecca; Wild, Johannes; Ringen, Julia; Karbach, Susanne; Wenzel, Philip

doi:10.1093/ajh/hpaa145

Cited by 4 publications

(2 citation statements)

References 153 publications

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“…In the past years, evidence has suggested that AH is, at least partially, an immunemediated inflammatory disorder. AH is shown to be associated with the accumulation of immune cells into the kidneys, which impede vascular relaxation and enhance sodium reabsorption, mediating sodium sensitivity and tissue injury [39].…”

Section: Innate Immunity Response and Oxidative Stressmentioning

confidence: 99%

Non-Haemodynamic Mechanisms Underlying Hypertension-Associated Damage in Target Kidney Components

Russo¹,

Bussalino

Macciò

et al. 2023

IJMS

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Arterial hypertension (AH) is a global challenge that greatly impacts cardiovascular morbidity and mortality worldwide. AH is a major risk factor for the development and progression of kidney disease. Several antihypertensive treatment options are already available to counteract the progression of kidney disease. Despite the implementation of the clinical use of renin–angiotensin aldosterone system (RAAS) inhibitors, gliflozins, endothelin receptor antagonists, and their combination, the kidney damage associated with AH is far from being resolved. Fortunately, recent studies on the molecular mechanisms of AH-induced kidney damage have identified novel potential therapeutic targets. Several pathophysiologic pathways have been shown to play a key role in AH-induced kidney damage, including inappropriate tissue activation of the RAAS and immunity system, leading to oxidative stress and inflammation. Moreover, the intracellular effects of increased uric acid and cell phenotype transition showed their link with changes in kidney structure in the early phase of AH. Emerging therapies targeting novel disease mechanisms could provide powerful approaches for hypertensive nephropathy management in the future. In this review, we would like to focus on the interactions of pathways linking the molecular consequences of AH to kidney damage, suggesting how old and new therapies could aim to protect the kidney.

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Section: Innate Immunity Response and Oxidative Stressmentioning

confidence: 99%

Non-Haemodynamic Mechanisms Underlying Hypertension-Associated Damage in Target Kidney Components

Russo¹,

Bussalino

Macciò

et al. 2023

IJMS

View full text Add to dashboard Cite

show abstract

“… 1 , 2 , 3 Many innate and adaptive immune cells have been defined to play a critical role in the development of hypertension. 4 , 5 , 6 , 7 , 8 For example, both innate immune cells, including monocytes, macrophages, dendritic cells, and myeloid‐derived suppressor cells, 9 , 10 and adaptive immune cells, including CD8 + T cells, CD4 + cells (T‐helper cells [Th] 1, Th2, Th17, and T‐regulatory [Treg] cells), and B cells can promote or inhibit hypertension. 11 , 12 In addition, a small subset of innate‐like T cells that express the γδ T‐cell receptor rather than the αβ T‐cell receptor is involved in angiotensin II (Ang II)–induced hypertension, vascular injury, and T‐cell activation.…”

mentioning

confidence: 99%

CD1d‐Dependent Natural Killer T Cells Mediate Hypertension and Vascular Injury Through Interleukin‐17A

Xiao,

Hou,

Zhang

et al. 2023

JAHA

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Background Different T‐lymphocyte subsets, including CD1d‐dependent natural killer T (NKT) cells, play distinct roles in hypertension, highlighting the importance of identifying key immune cells for its treatment. This study aimed to determine the unknown effects of CD1d‐dependent NKT cells on hypertension and vascular injury. Methods and Results Hypertension models were induced in male CD1d knockout (CD1dko), wild‐type, and adoptive bone marrow transfer mice by angiotensin II (Ang II) or deoxycorticosterone acetate salt. Blood pressure was measured by the tail‐cuff system and radiotelemetry. Vascular injury was assessed by histologic studies or aortic ring assay. Inflammation was detected by flow cytometry, quantitative real‐time polymerase chain reaction, or ELISA. Results showed that Ang II infusion significantly reduced CD1d expression and NKT cell numbers in the aorta of mice. CD1dko mice exhibited worsened blood pressure elevation, vascular injury, and inflammatory response induced by Ang II or deoxycorticosterone acetate salt. However, these effects were markedly reversed in wild‐type mice treated with NKT cell–specific activator. Adoptive transfer of CD1dko bone marrow cells to wild‐type mice also significantly worsened Ang II–induced responses. Mechanistically, CD1dko increased Ang II–induced interleukin‐6 production and activated signal transducer and activator of transcription 3 and orphan nuclear receptor γ, subsequently inducing interleukin‐17A production. Neutralizing interleukin‐17A partially reversed Ang II–induced hypertension and vascular injury in CD1dko mice. In addition, levels of NKT cells were lower in the blood of patients with hypertension (n=57) compared with normotensive individuals (n=87). Conclusions These findings reveal a previously unknown role for CD1d‐dependent NKT cells in hypertension and vascular injury, indicating that NKT cell activation could be a promising therapeutic target for hypertension.

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Reactive Oxygen Species Scavenging Nanomedicine for the Treatment of Ischemic Heart Disease

Zhang

Dalan

et al. 2022

Advanced Materials

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Ischemic heart disease (IHD) is the leading cause of disability and mortality worldwide. Reactive oxygen species (ROS) have been shown to play key roles in the progression of diabetes, hypertension, and hypercholesterolemia, which are independent risk factors that lead to atherosclerosis and the development of IHD. Engineered biomaterial‐based nanomedicines are under extensive investigation and exploration, serving as smart and multifunctional nanocarriers for synergistic therapeutic effect. Capitalizing on cell/molecule‐targeting drug delivery, nanomedicines present enhanced specificity and safety with favorable pharmacokinetics and pharmacodynamics. Herein, the roles of ROS in both IHD and its risk factors are discussed, highlighting cardiovascular medications that have antioxidant properties, and summarizing the advantages, properties, and recent achievements of nanomedicines that have ROS scavenging capacity for the treatment of diabetes, hypertension, hypercholesterolemia, atherosclerosis, ischemia/reperfusion, and myocardial infarction. Finally, the current challenges of nanomedicines for ROS‐scavenging treatment of IHD and possible future directions are discussed from a clinical perspective.

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Innate Immune Mechanisms of Arterial Hypertension and Autoimmune Disease

Cited by 4 publications

References 153 publications

Non-Haemodynamic Mechanisms Underlying Hypertension-Associated Damage in Target Kidney Components

Non-Haemodynamic Mechanisms Underlying Hypertension-Associated Damage in Target Kidney Components

CD1d‐Dependent Natural Killer T Cells Mediate Hypertension and Vascular Injury Through Interleukin‐17A

Reactive Oxygen Species Scavenging Nanomedicine for the Treatment of Ischemic Heart Disease

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