Evidence map›Paper›PMID 25552697›Full record

ReviewCirculation research2015

Role of mineralocorticoid receptor antagonists in cardiovascular disease.

Carlos M Ferrario, Ernesto L Schiffrin

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
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 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
6.7field-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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Vascular (dys)function in the failing heart.Nature reviews. Cardiology · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Role of NaInternational journal of molecular sciences · 2024
    Review
  16. Review
  17. Article
  18. Impact of ovary-intact menopause in a mouse model of heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  19. Review
  20. Article
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

2 authors at 1 institution in 1 country.

Carlos M FerrarioFrom the Hypertension Translational Research Laboratory, Departments of Surgery, Internal Medicine-Nephrology, and Physiology-Pharmacology, Wake Forest University Health Science Center, Winston Salem, NC (C.M.F.); and Department of Medicine and Lady Davis Institute for Medical Research, SMBD-Jewish General Hospital, McGill University, Montreal, PQ, Canada (E.L.S.). cferrari@wakehealth.edu.
Ernesto L SchiffrinFrom the Hypertension Translational Research Laboratory, Departments of Surgery, Internal Medicine-Nephrology, and Physiology-Pharmacology, Wake Forest University Health Science Center, Winston Salem, NC (C.M.F.); and Department of Medicine and Lady Davis Institute for Medical Research, SMBD-Jewish General Hospital, McGill University, Montreal, PQ, Canada (E.L.S.).
Jewish General Hospital · CA

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI GROBAN, LEANNE · 1994 to 2019
$34.8M
Canadian Institutes of Health Research 102606Canadian Institutes of Health Research 37917Canadian Institutes of Health Research 82790NHLBI NIH HHS HL-051952NHLBI NIH HHS P01 HL051952
6 · The paper itself

Abstract

Aldosterone exerts its best known sodium homeostasis actions by controlling sodium excretion at the level of the distal tubules via activation of the apical epithelial sodium channel and the basolateral Na(+)/K(+)ATPase pump. Recently, this mineralocorticoid hormone has been demonstrated to act on the heart and blood vessels. Excess release of aldosterone in relation to the salt status induces both genomic and nongenomic effects that by promoting endothelial dysfunction, and vascular and cardiorenal adverse remodeling, contribute to the target organ damage found in hypertension, heart failure, myocardial infarction, and chronic renal failure. Mineralocorticoid receptor blockers have been shown to be highly effective in resistant hypertension and to slow down heart failure progression, and in experimental animals, the development of atherosclerosis. Blockade of the action of aldosterone and potentially other mineralocorticoid steroids has been increasingly demonstrated to be an extremely beneficial therapy in different forms of cardiovascular disease. This review provides a summary of the knowledge that exists on aldosterone actions in the cardiovascular system and, in providing the translational impact of this knowledge to the clinical arena, illustrates how much more needs to be achieved in exploring the use of mineralocorticoid receptor blockers in less advanced stages of heart, renal, and vascular disease.

Indexed as

AldosteroneAnimalsCardiovascular DiseasesHomeostasisHumansMineralocorticoid Receptor AntagonistsReceptors, MineralocorticoidAldosteroneMineralocorticoid Receptor AntagonistsReceptors, Mineralocorticoidheart failurehypertensionkidney failure, chronic

Identifiers

PMID25552697
PMCPMC4283558
OpenAlexW2107968545

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.