Evidence map›Paper›PMID 28637706›Full record

ArticlePhysiological reports2017

Endothelial mineralocorticoid receptor contributes to systolic dysfunction induced by pressure overload without modulating cardiac hypertrophy or inflammation.

Ane M Salvador, M Elizabeth Moss, Mark Aronovitz, Kathleen B Mueller, Robert M Blanton, Iris Z Jaffe, Pilar Alcaide

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  7. Capillaries as a Therapeutic Target for Heart Failure.Journal of atherosclerosis and thrombosis · 2022
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Pathophysiological mechanisms of mineralocorticoid receptor-dependent cardiovascular and chronic kidney disease.Hypertension research : official journal of the Japanese Society of Hypertension · 2019
    Review
  14. Review
  15. Article
  16. Article
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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

7 authors at 2 institutions in 2 countries.

Ane M SalvadorDepartment of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, Massachusetts.
M Elizabeth MossSackler School of Biomedical Sciences, Tufts University School of Medicine, Boston, Massachusetts.
Mark AronovitzMolecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts.
Kathleen B MuellerSackler School of Biomedical Sciences, Tufts University School of Medicine, Boston, Massachusetts.
Robert M BlantonMolecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts.
Iris Z JaffeMolecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts.
Pilar AlcaideDepartment of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, Massachusetts pilar.alcaide@tufts.edu.
Tufts Medical Center · USTufts 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
T Cell Mediated Immune Responses as a Regulator of Heart FailureR01HL123658 · NHLBI · TUFTS UNIVERSITY BOSTON · PI ALCAIDE ALONSO, MARIA PILAR · 2014 to 2018
$2.2M
Novel Protein Kinase GI Substrates in Cardiac Remodeling and Blood Pressure ControlR01HL131831 · NHLBI · TUFTS MEDICAL CENTER · PI BLANTON, ROBERT MORRIS · 2016 to 2020
$2.1M
NHLBI NIH HHS R01 HL095590NHLBI NIH HHS R01 HL123658NHLBI NIH HHS R01 HL131831
6 · The paper itself

Abstract

Heart Failure (HF) is associated with increased circulating levels of aldosterone and systemic inflammation. Mineralocorticoid receptor (MR) antagonists block aldosterone action and decrease mortality in patients with congestive HF However, the molecular mechanisms underlying the therapeutic benefits of MR antagonists remain unclear. MR is expressed in all cell types in the heart, including the endothelial cells (EC), in which aldosterone induces the expression of intercellular adhesion molecule 1 (ICAM-1). Recently, we reported that ICAM-1 regulates cardiac inflammation and cardiac function in mice subjected to transverse aortic constriction (TAC). Whether MR specifically in endothelial cells (EC) contributes to the several mechanisms of pathological cardiac remodeling and cardiac dysfunction remains unclear. Basal cardiac function and LV dimensions were comparable in mice with MR selectively deleted from ECs (EC-MR

Indexed as

SystoleVentricular DysfunctionAnimalsCardiomegalyCells, CulturedEndothelium, VascularFibrosisInflammationIntercellular Adhesion Molecule-1MaleMiceMice, Inbred C57BLReceptors, MineralocorticoidTumor Necrosis Factor-alphaVentricular RemodelingIntercellular Adhesion Molecule-1Receptors, MineralocorticoidTumor Necrosis Factor-alphaAdhesion moleculesendothelial cellheart failureinflammationmineralocorticoid receptor

Identifiers

PMID28637706
PMCPMC5492203
OpenAlexW2682751735

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.