PortalPublikationenImmune Mechanisms in Arterial Hypertension

Immune Mechanisms in Arterial Hypertension

Standard

Immune Mechanisms in Arterial Hypertension. / Wenzel, Ulrich; Turner, Jan Eric; Krebs, Christian; Kurts, Christian; Harrison, David G; Ehmke, Heimo.

in: J AM SOC NEPHROL, Jahrgang 27, Nr. 3, 03.2016, S. 677-86.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Wenzel, U, Turner, JE, Krebs, C, Kurts, C, Harrison, DG & Ehmke, H 2016, 'Immune Mechanisms in Arterial Hypertension', J AM SOC NEPHROL, Jg. 27, Nr. 3, S. 677-86. https://doi.org/10.1681/ASN.2015050562

APA

Wenzel, U., Turner, J. E., Krebs, C., Kurts, C., Harrison, D. G., & Ehmke, H. (2016). Immune Mechanisms in Arterial Hypertension. J AM SOC NEPHROL, 27(3), 677-86. https://doi.org/10.1681/ASN.2015050562

Vancouver

Wenzel U, Turner JE, Krebs C, Kurts C, Harrison DG, Ehmke H. Immune Mechanisms in Arterial Hypertension. J AM SOC NEPHROL. 2016 Mär;27(3):677-86. https://doi.org/10.1681/ASN.2015050562

Bibtex

@article{ba2ad7827fdc42d79374ff35f2d9cac3,
title = "Immune Mechanisms in Arterial Hypertension",
abstract = "Traditionally, arterial hypertension and subsequent end-organ damage have been attributed to hemodynamic factors, but increasing evidence indicates that inflammation also contributes to the deleterious consequences of this disease. The immune system has evolved to prevent invasion of foreign organisms and to promote tissue healing after injury. However, this beneficial activity comes at a cost of collateral damage when the immune system overreacts to internal injury, such as prehypertension. Renal inflammation results in injury and impaired urinary sodium excretion, and vascular inflammation leads to endothelial dysfunction, increased vascular resistance, and arterial remodeling and stiffening. Notably, modulation of the immune response can reduce the severity of BP elevation and hypertensive end-organ damage in several animal models. Indeed, recent studies have improved our understanding of how the immune response affects the pathogenesis of arterial hypertension, but the remarkable advances in basic immunology made during the last few years still await translation to the field of hypertension. This review briefly summarizes recent advances in immunity and hypertension as well as hypertensive end-organ damage.",
author = "Ulrich Wenzel and Turner, {Jan Eric} and Christian Krebs and Christian Kurts and Harrison, {David G} and Heimo Ehmke",
note = "Copyright {\textcopyright} 2016 by the American Society of Nephrology.",
year = "2016",
month = mar,
doi = "10.1681/ASN.2015050562",
language = "English",
volume = "27",
pages = "677--86",
journal = "J AM SOC NEPHROL",
issn = "1046-6673",
publisher = "American Society of Nephrology",
number = "3",

}

RIS

TY - JOUR

T1 - Immune Mechanisms in Arterial Hypertension

AU - Wenzel, Ulrich

AU - Turner, Jan Eric

AU - Krebs, Christian

AU - Kurts, Christian

AU - Harrison, David G

AU - Ehmke, Heimo

N1 - Copyright © 2016 by the American Society of Nephrology.

PY - 2016/3

Y1 - 2016/3

N2 - Traditionally, arterial hypertension and subsequent end-organ damage have been attributed to hemodynamic factors, but increasing evidence indicates that inflammation also contributes to the deleterious consequences of this disease. The immune system has evolved to prevent invasion of foreign organisms and to promote tissue healing after injury. However, this beneficial activity comes at a cost of collateral damage when the immune system overreacts to internal injury, such as prehypertension. Renal inflammation results in injury and impaired urinary sodium excretion, and vascular inflammation leads to endothelial dysfunction, increased vascular resistance, and arterial remodeling and stiffening. Notably, modulation of the immune response can reduce the severity of BP elevation and hypertensive end-organ damage in several animal models. Indeed, recent studies have improved our understanding of how the immune response affects the pathogenesis of arterial hypertension, but the remarkable advances in basic immunology made during the last few years still await translation to the field of hypertension. This review briefly summarizes recent advances in immunity and hypertension as well as hypertensive end-organ damage.

AB - Traditionally, arterial hypertension and subsequent end-organ damage have been attributed to hemodynamic factors, but increasing evidence indicates that inflammation also contributes to the deleterious consequences of this disease. The immune system has evolved to prevent invasion of foreign organisms and to promote tissue healing after injury. However, this beneficial activity comes at a cost of collateral damage when the immune system overreacts to internal injury, such as prehypertension. Renal inflammation results in injury and impaired urinary sodium excretion, and vascular inflammation leads to endothelial dysfunction, increased vascular resistance, and arterial remodeling and stiffening. Notably, modulation of the immune response can reduce the severity of BP elevation and hypertensive end-organ damage in several animal models. Indeed, recent studies have improved our understanding of how the immune response affects the pathogenesis of arterial hypertension, but the remarkable advances in basic immunology made during the last few years still await translation to the field of hypertension. This review briefly summarizes recent advances in immunity and hypertension as well as hypertensive end-organ damage.

U2 - 10.1681/ASN.2015050562

DO - 10.1681/ASN.2015050562

M3 - SCORING: Journal article

C2 - 26319245

VL - 27

SP - 677

EP - 686

JO - J AM SOC NEPHROL

JF - J AM SOC NEPHROL

SN - 1046-6673

IS - 3

ER -