Role of T-cell activation in salt-sensitive hypertension

Ren, Jiafa; Crowley, Steven D.

doi:10.1152/ajpheart.00096.2019

Cited by 31 publications

(27 citation statements)

References 62 publications

(69 reference statements)

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“…In cellular immunity, activated T lymphocytes have been illuminated to raise blood pressure by inducing oxidative stress injury and renal reabsorption of sodium. On the other hand, the lack of T cells in animals has been observed to reduce oxidative stress and RAS activation, causing lower blood pressure [17]. In our study, higher When Adj.…”

Section: Discussionsupporting

confidence: 41%

Pathogenesis of Higher Blood Pressure and Worse Renal Function in Salt-Sensitive Hypertension

Chu¹,

Zhou²,

Lu³

et al. 2021

Kidney Blood Press Res

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Background: The underlying pathogenesis of patients with salt-sensitive hypertension expressing higher blood pressure and severer renal damage remains uncertain. Methods: We recruited 329 subjects, 131 in salt-sensitive (SS) group, 148 in nonsalt-sensitive (NSS) group, and 50 healthy people in normal group and tested their renal function, 24-h ambulatory blood pressure, and growth factor series. Results: The SS group showed worse renal function with lower estimated glomerular filtration rate and higher urinary microalbumin, α-microglobulin, urinary protein Cr ratio, and urinary immunoglobulin. Most indicators in 24-h ambulatory blood pressure of the SS group were significantly enhanced than the NSS group, indicating their higher blood pressure. The significantly elevated growth factors in the SS group were AR, BMP-5, EG-VEGF, GH, HGF, IGFBP-2, IGFBP-3, IGFBP-6, MCSFR, NT-4, PDGF-AA, SCF, SCFR, VEGFR2, VEGFR3, and VEGF-D, compared to other 2 groups or one of them. PI3K-AKT pathway was activated in the SS group. Conclusions: Differences in growth factors and pathways may account for the manifestations of the SS group. Activated PI3K-AKT pathway with higher IGFBP-3 and GH can lead to renal damage. Higher MCSFR in the SS group indicates that high blood pressure and severe kidney damage may be associated with the activation of the immune system. EG-VEGF, VEGFR2, VEGFR3, and VEGF-D can also explain the elevated blood pressure due to the dilated lymphatic system which drains excess sodium and water back into circulation. The SS group presented higher AR and HGF which may worsen renal function by regulating cell proliferation and tumor formation. However, due to the potential low awareness rate of hypertension at the very beginning, we cannot ensure the exact occurrence order of blood pressure, renal damage, and salt sensitivity. Therefore, further studies which can track data from the onset of hypertension are needed.

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Section: Discussionsupporting

confidence: 41%

Pathogenesis of Higher Blood Pressure and Worse Renal Function in Salt-Sensitive Hypertension

Chu¹,

Zhou²,

Lu³

et al. 2021

Kidney Blood Press Res

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“…In addition, hypertension in humans is associated with elevated plasma C3a and C5a concentrations and reduced FOXP3+ Treg counts 54,57 and thus, an analogous mechanism may occur in humans. However, although this antihypertensive effect is linked to anti‐inflammatory cytokine production (e.g., IL‐10 and TGF‐β) and reduced blood vessel infiltration by macrophages, its full nature is incompletely understood 58,59 . This and other emerging studies suggest complement is a key regulator of the innate and adaptive immune system in hypertension 57,60–62 …”

Section: Hypertensionmentioning

confidence: 99%

Complement: Bridging the innate and adaptive immune systems in sterile inflammation

Woodruff

2020

Journal of Leukocyte Biology

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The complement system is a collection of soluble and membrane‐bound proteins that together act as a powerful amplifier of the innate and adaptive immune systems. Although its role in infection is well established, complement is becoming increasingly recognized as a key contributor to sterile inflammation, a chronic inflammatory process often associated with noncommunicable diseases. In this context, damaged tissues release danger signals and trigger complement, which acts on a range of leukocytes to augment and bridge the innate and adaptive immune systems. Given the detrimental effect of chronic inflammation, the complement system is therefore well placed as an anti‐inflammatory drug target. In this review, we provide a general outline of the sterile activators, effectors, and targets of the complement system and a series of examples (i.e., hypertension, cancer, allograft transplant rejection, and neuroinflammation) that highlight complement's ability to bridge the 2 arms of the immune system.

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“…Hypertension and kidney disease are associated with the accumulation of T cells, monocyte/macrophages, and T cell–derived cytokines in the kidney [ 129 ]. An imbalance of T regulatory cells (Treg) and T helper 17 (TH17) cells has been associated with hypertension [ 130 ], which can be protected by restoration the balance of Treg/TH17 by postbiotic therapy [ 131 ]. In CKD, the interplay between Treg/TH17 balance and inflammation has also been associated with hypertension and the progression of CKD [ 132 ].…”

Section: Common Mechanisms Link Tryptophan Metabolism To Developmementioning

confidence: 99%

Developmental Programming and Reprogramming of Hypertension and Kidney Disease: Impact of Tryptophan Metabolism

Hsu

Tain

2020

IJMS

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The concept that hypertension and chronic kidney disease (CKD) originate in early life has emerged recently. During pregnancy, tryptophan is crucial for maternal protein synthesis and fetal development. On one hand, impaired tryptophan metabolic pathway in pregnancy impacts fetal programming, resulting in the developmental programming of hypertension and kidney disease in adult offspring. On the other hand, tryptophan-related interventions might serve as reprogramming strategies to prevent a disease from occurring. In the present review, we aim to summarize (1) the three major tryptophan metabolic pathways, (2) the impact of tryptophan metabolism in pregnancy, (3) the interplay occurring between tryptophan metabolites and gut microbiota on the production of uremic toxins, (4) the role of tryptophan-derived metabolites-induced hypertension and CKD of developmental origin, (5) the therapeutic options in pregnancy that could aid in reprogramming adverse effects to protect offspring against hypertension and CKD, and (6) possible mechanisms linking tryptophan metabolism to developmental programming of hypertension and kidney disease.

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Role of T-cell activation in salt-sensitive hypertension

Cited by 31 publications

References 62 publications

Pathogenesis of Higher Blood Pressure and Worse Renal Function in Salt-Sensitive Hypertension

Pathogenesis of Higher Blood Pressure and Worse Renal Function in Salt-Sensitive Hypertension

Complement: Bridging the innate and adaptive immune systems in sterile inflammation

Developmental Programming and Reprogramming of Hypertension and Kidney Disease: Impact of Tryptophan Metabolism

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