Evidence map›Paper›PMID 25767287›Full record

ReviewCirculation research2015

Inflammation, immunity, and hypertensive end-organ damage.

William G McMaster, Annet Kirabo, Meena S Madhur, David G Harrison

Abstract readReview
In one paragraph

Review in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 420 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
420citing papers in PubMed, 5 pooled it
49.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

420 citing papers in PubMed, 5 syntheses or guidelines pooled it, 690 citations in OpenAlex.

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360 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

William G McMasterFrom the Department of Surgery, Division of Clinical Pharmacology (W.G.M.) and the Department of Medicine (W.G.M., A.K., M.S.M., D.G.H.), Vanderbilt University School of Medicine, Nashville, TN.
Annet KiraboFrom the Department of Surgery, Division of Clinical Pharmacology (W.G.M.) and the Department of Medicine (W.G.M., A.K., M.S.M., D.G.H.), Vanderbilt University School of Medicine, Nashville, TN.
Meena S MadhurFrom the Department of Surgery, Division of Clinical Pharmacology (W.G.M.) and the Department of Medicine (W.G.M., A.K., M.S.M., D.G.H.), Vanderbilt University School of Medicine, Nashville, TN.
David G HarrisonFrom the Department of Surgery, Division of Clinical Pharmacology (W.G.M.) and the Department of Medicine (W.G.M., A.K., M.S.M., D.G.H.), Vanderbilt University School of Medicine, Nashville, TN. david.g.harrison@vanderbilt.edu.
Vanderbilt University · US

Funding

Vascular specific ACE expression and atherosclerosisP01HL058000 · NHLBI · VANDERBILT UNIVERSITY · PI DIKALOV, SERGEY · 1998 to 2013
$20.7M
T cell triggering events and hypertensionP01HL095070 · NHLBI · EMORY UNIVERSITY · PI JO, HANJOONG · 2009 to 2019
$20.5M
Therapeutic Modulation of Endothelial Cell TetrahydrobiopterinP01GM015431 · NIGMS · VANDERBILT UNIVERSITY · PI ROBERTS, JACKSON L · 2011 to 2015
$9.5M
Immunobiology of Blood and Vascular Systems Training ProgramT32HL069765 · NHLBI · VANDERBILT UNIVERSITY · PI HAWIGER, JACK J · 2002 to 2016
$6.5M
REGULATION OF VASCULAR FUNCTION BY THE ENDOTHELIUMR01HL039006 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARRISON, DAVID G · 1987 to 2017
$5.5M
Role of Vascular Oxidative Stress in ObesityR01HL108701 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CAI, HUA LINDA, HARRISON, DAVID G · 2012 to 2015
$1.9M
Roles of oxidation and inflammation in aortic stiffeningR01HL105294 · NHLBI · VANDERBILT UNIVERSITY · PI HARRISON, DAVID G · 2010 to 2013
$1.5M
The Role of The T Cell In The Genesis of Hypertension R01HL125865 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARRISON, DAVID G · 2015 to 2017
$1.2M
Role of Salt, Isoketal-modified Proteins and Dendritic Cells in HypertensionK01HL130497 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KIRABO, ANNET · 2016 to 2020
$803k
Diverse Roles of Interleukin 17 Isoforms in the Pathogenesis of HypertensionK08HL121671 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MADHUR, MEENAKSHI SWAMINATHAN · 2014 to 2018
$723k
NHLBI NIH HHS K01 HL130497NHLBI NIH HHS K08 HL121671NHLBI NIH HHS K08HL121671NHLBI NIH HHS P01 HL058000NHLBI NIH HHS P01HL058000NHLBI NIH HHS P01 HL095070NHLBI NIH HHS P01HL095070NHLBI NIH HHS R01 HL039006NHLBI NIH HHS R01HL039006NHLBI NIH HHS R01 HL105294NHLBI NIH HHS R01HL105294NHLBI NIH HHS R01 HL108701NHLBI NIH HHS R01HL108701NHLBI NIH HHS R01 HL125865NHLBI NIH HHS T32 HL069765NHLBI NIH HHS T32 HL69765NIGMS NIH HHS P01 GM015431NIGMS NIH HHS P01GM015431
6 · The paper itself

Abstract

For >50 years, it has been recognized that immunity contributes to hypertension. Recent data have defined an important role of T cells and various T cell-derived cytokines in several models of experimental hypertension. These studies have shown that stimuli like angiotensin II, deoxycorticosterone acetate-salt, and excessive catecholamines lead to formation of effector like T cells that infiltrate the kidney and perivascular regions of both large arteries and arterioles. There is also accumulation of monocyte/macrophages in these regions. Cytokines released from these cells, including interleukin-17, interferon-γ, tumor necrosis factorα, and interleukin-6 promote both renal and vascular dysfunction and damage, leading to enhanced sodium retention and increased systemic vascular resistance. The renal effects of these cytokines remain to be fully defined, but include enhanced formation of angiotensinogen, increased sodium reabsorption, and increased renal fibrosis. Recent experiments have defined a link between oxidative stress and immune activation in hypertension. These have shown that hypertension is associated with formation of reactive oxygen species in dendritic cells that lead to formation of gamma ketoaldehydes, or isoketals. These rapidly adduct to protein lysines and are presented by dendritic cells as neoantigens that activate T cells and promote hypertension. Thus, cells of both the innate and adaptive immune system contribute to end-organ damage and dysfunction in hypertension. Therapeutic interventions to reduce activation of these cells may prove beneficial in reducing end-organ damage and preventing consequences of hypertension, including myocardial infarction, heart failure, renal failure, and stroke.

Indexed as

Adaptive ImmunityAnimalsBenzylaminesCardiovascular DiseasesCytokinesDrug Evaluation, PreclinicalHumansHypertensionImmunity, InnateInflammationKidneyLymphocyte ActivationMiceMice, KnockoutModels, AnimalModels, Cardiovascular2-(aminomethyl)phenolBenzylaminesCytokinesReactive Oxygen Speciesangiotensin IIantigen presenting cellcytokineseffector T cellnitric oxide synthasesodium

Identifiers

PMID25767287
PMCPMC4535695
OpenAlexW2155504581

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.