Evidence map›Paper›PMID 20697155›Full record

ArticleThe Journal of clinical investigation2010

Myeloid mineralocorticoid receptor controls macrophage polarization and cardiovascular hypertrophy and remodeling in mice.

Michael G Usher, Sheng Zhong Duan, Christine Y Ivaschenko, Ryan A Frieler, Stefan Berger, Günther Schütz, Carey N Lumeng, Richard M Mortensen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
187citing papers in PubMed, 2 pooled it
16.6field-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

187 citing papers in PubMed, 2 syntheses or guidelines pooled it, 376 citations in OpenAlex.

  1. Pooled it
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  5. Salt and chronic kidney disease.Nature reviews. Nephrology · 2026
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127 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

8 authors at 2 institutions in 2 countries.

Michael G UsherDepartment of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan 48109-5622, USA.
Sheng Zhong Duan
Christine Y Ivaschenko
Ryan A Frieler
Stefan Berger
Günther Schütz
Carey N Lumeng
Richard M Mortensen
University of Michigan–Ann Arbor · USGerman Cancer Research Center · DE

Funding

Metabolic responsive factors in cardiovascular diseaseR01HL083201 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MORTENSEN, RICHARD M · 2006 to 2009
$1.5M
Adipose tissue macrophage polarization and its influence on adipocyte functionK08DK078851 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUMENG, CAREY N · 2007 to 2011
$705k
NHLBI NIH HHS R01 HL083201NHLBI NIH HHS R01HL083201
6 · The paper itself

Abstract

Inappropriate excess of the steroid hormone aldosterone, which is a mineralocorticoid receptor (MR) agonist, is associated with increased inflammation and risk of cardiovascular disease. MR antagonists are cardioprotective and antiinflammatory in vivo, and evidence suggests that they mediate these effects in part by aldosterone-independent mechanisms. Here we have shown that MR on myeloid cells is necessary for efficient classical macrophage activation by proinflammatory cytokines. Macrophages from mice lacking MR in myeloid cells (referred to herein as MyMRKO mice) exhibited a transcription profile of alternative activation. In vitro, MR deficiency synergized with inducers of alternatively activated macrophages (for example, IL-4 and agonists of PPARgamma and the glucocorticoid receptor) to enhance alternative activation. In vivo, MR deficiency in macrophages mimicked the effects of MR antagonists and protected against cardiac hypertrophy, fibrosis, and vascular damage caused by L-NAME/Ang II. Increased blood pressure and heart rates and decreased circadian variation were observed during treatment of MyMRKO mice with L-NAME/Ang II. We conclude that myeloid MR is an important control point in macrophage polarization and that the function of MR on myeloid cells likely represents a conserved ancestral MR function that is integrated in a transcriptional network with PPARgamma and glucocorticoid receptor. Furthermore, myeloid MR is critical for blood pressure control and for hypertrophic and fibrotic responses in the mouse heart and aorta.

Indexed as

Mineralocorticoid Receptor AntagonistsAldosteroneAnimalsBlood PressureCardiomegalyCardiovascular DiseasesFibrosisHeartHypertensionHypertrophyInterleukin-4MacrophagesMiceMice, KnockoutMice, TransgenicNG-Nitroarginine Methyl EsterAldosteroneInterleukin-4Mineralocorticoid Receptor AntagonistsNG-Nitroarginine Methyl EsterNR3C1 protein, humanReceptors, GlucocorticoidReceptors, Mineralocorticoid

Identifiers

PMID20697155
PMCPMC2929712
OpenAlexW1965301500

What OpenQuestion holds

Textmetadata
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.