Evidence map›Paper›PMID 24769248›Full record

ReviewSteroids2014

Mineralocorticoid receptors in immune cells: emerging role in cardiovascular disease.

Nicholas C Bene, Pilar Alcaide, Henry H Wortis, Iris Z Jaffe

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Steroids, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

65 citing papers in PubMed, 99 citations in OpenAlex.

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5 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.

Nicholas C BeneTufts University School of Medicine, Boston, MA, USA.
Pilar AlcaideTufts University School of Medicine, Boston, MA, USA; Sackler School of Graduate Biomedical Sciences, Boston, MA, USA; Tufts Medical Center, Molecular Cardiology Research Institute, Boston, MA, USA.
Henry H WortisTufts University School of Medicine, Boston, MA, USA; Sackler School of Graduate Biomedical Sciences, Boston, MA, USA.
Iris Z JaffeTufts University School of Medicine, Boston, MA, USA; Sackler School of Graduate Biomedical Sciences, Boston, MA, USA; Tufts Medical Center, Molecular Cardiology Research Institute, Boston, MA, USA. Electronic address: ijaffe@tuftsmedicalcenter.org.
Tufts University · US

Funding

The Role of Vascular MR-Regulated Genes in Vascular Function and DiseaseR01HL095590 · NHLBI · TUFTS MEDICAL CENTER · PI Iris Z Jaffe · 2009 to 2026
$7.7M
Endothelial regulation of IL17 producing T effector cell migrationR00HL094706 · NHLBI · TUFTS MEDICAL CENTER · PI ALCAIDE ALONSO, MARIA PILAR · 2011 to 2013
$735k
Endothelial regulation of IL17 producing T effector cell migrationK99HL094706 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI ALCAIDE ALONSO, MARIA PILAR · 2009 to 2010
$277k
NHLBI NIH HHS HL094706NHLBI NIH HHS HL095590-05NHLBI NIH HHS K99 HL094706NHLBI NIH HHS R00 HL094706NHLBI NIH HHS R01 HL095590
6 · The paper itself

Abstract

Mineralocorticoid receptors (MRs) contribute to the pathophysiology of hypertension and cardiovascular disease in humans. As such, MR antagonists improve cardiovascular outcomes but the molecular mechanisms remain unclear. The actions of the MR in the kidney to increase blood pressure are well known, but the recent identification of MRs in immune cells has led to novel discoveries in the pathogenesis of cardiovascular disease that are reviewed here. MR regulates macrophage activation to the pro-inflammatory M1 phenotype and this process contributes to the pathogenesis of cardiovascular fibrosis in response to hypertension and to outcomes in mouse models of stroke. T lymphocytes have recently been implicated in the development of hypertension and cardiovascular fibrosis in mouse models. MR activation in vivo promotes T lymphocyte differentiation to the pro-inflammatory Th1 and Th17 subsets while decreasing the number of anti-inflammatory T regulatory lymphocytes. The mechanism likely involves activation of MR in antigen presenting dendritic cells that subsequently regulate Th1/Th17 polarization by production of cytokines. Alteration of the balance between T helper and T regulatory lymphocytes contributes to the pathogenesis of hypertension and atherosclerosis and the associated complications. B lymphocytes also express the MR and specific B lymphocyte-derived antibodies modulate the progression of atherosclerosis. However, the role of MR in B lymphocyte function remains to be explored. Overall, recent studies of MR in immune cells have identified new mechanisms by which MR activation may contribute to the pathogenesis of organ damage in patients with cardiovascular risk factors. Conversely, inhibition of leukocyte MR may contribute to the protective effects of MR antagonist drugs in cardiovascular patients. Further understanding of the role of MR in leukocyte function could yield novel drug targets for cardiovascular disease.

Indexed as

AnimalsCardiovascular DiseasesHumansLeukocytesModels, BiologicalReceptors, MineralocorticoidRenin-Angiotensin SystemReceptors, MineralocorticoidAldosteroneCardiovascular diseaseHypertensionMacrophageMineralocorticoid receptorT lymphocyte

Identifiers

PMID24769248
PMCPMC4205205
OpenAlexW1985307512

What OpenQuestion holds

Textmetadata
LicenceTDM
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.