Evidence map›Paper›PMID 23774812›Full record

ReviewNature reviews. Nephrology2013

Contribution of aldosterone to cardiovascular and renal inflammation and fibrosis.

Nancy J Brown

Registry-linked trialAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02948998 (Evaluating the Effect of Spironolactone on Hypertrophic Cardiomyopathy-- a Multicenter Randomized Control Trial), which is not on this map. Cited by 242 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
242citing papers in PubMed, 5 pooled it
–field-weighted citation impact
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.

NCT02948998 phase4unknown statusnot on this mapstarted 2018, after this paper: background citation

Evaluating the Effect of Spironolactone on Hypertrophic Cardiomyopathy-- a Multicenter Randomized Control Trial

TypeinterventionalSponsorXinhua Hospital, Shanghai Jiao Tong University School of MedicineRan2018 to 2020Enrolled260ConditionsHypertrophic Cardiomyopathy, FibrosisArmsSpironolactone
3 · Its place in the literature

Who cites it

242 citing papers in PubMed, 5 syntheses or guidelines pooled it.

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182 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

1 author.

Nancy J BrownVanderbilt University School of Medicine, Nashville, TN 37232, USA. nancy.j.brown@vanderbilt.edu

Funding

RENIN/ANGIOTENSIN SYSTEM AND FIBRINOLYSIS IN HUMANSR01HL060906 · NHLBI · VANDERBILT UNIVERSITY · PI BROWN, NANCY J. · 1998 to 2014
$5.4M
NHLBI NIH HHS HL060906NHLBI NIH HHS R01 HL060906
6 · The paper itself

Abstract

The steroid hormone aldosterone regulates sodium and potassium homeostasis. Aldosterone and activation of the mineralocorticoid receptor also causes inflammation and fibrosis of the heart, fibrosis and remodelling of blood vessels and tubulointerstitial fibrosis and glomerular injury in the kidney. Aldosterone and mineralocorticoid-receptor activation initiate an inflammatory response by increasing the generation of reactive oxygen species by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and mitochondria. High salt intake potentiates these effects, in part by activating the Rho family member Rac1, a regulatory subunit of reduced NADPH oxidase that activates the mineralocorticoid receptor. Studies in mice in which the mineralocorticoid receptor has been deleted from specific cell types suggest a key role for macrophages in promoting inflammation and fibrosis. Aldosterone can exert mineralocorticoid-receptor-independent effects via the angiotensin II receptor and via G-protein-coupled receptor 30. Mineralocorticoid-receptor antagonists are associated with decreased mortality in patients with heart disease and show promise in patients with kidney injury, but can elevate serum potassium concentration. Studies in rodents genetically deficient in aldosterone synthase or treated with a pharmacological aldosterone-synthase inhibitor are providing insight into the relative contribution of aldosterone compared with the contribution of mineralocorticoid-receptor activation in inflammation, fibrosis, and injury. Aldosterone-synthase inhibitors are under development in humans.

Indexed as

AldosteroneAnimalsAromatase InhibitorsCardiovascular SystemCytochrome P-450 CYP11B2Endothelial CellsFadrozoleFibrosisHumansImidazolesInflammationKidneyMacrophagesMineralocorticoid Receptor AntagonistsMyocardiumMyocytes, CardiacAldosteroneAromatase InhibitorsCytochrome P-450 CYP11B2FadrozoleImidazolesMineralocorticoid Receptor AntagonistsOsilodrostatPyridinesReactive Oxygen SpeciesReceptors, MineralocorticoidSodium, Dietary

Identifiers

PMID23774812
PMCPMC3922409

What OpenQuestion holds

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Registered trials

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.