Evidence map›Paper›PMID 37371584›Full record

ReviewBiomolecules2023

Aldosterone: Essential for Life but Damaging to the Vascular Endothelium.

Michael Crompton, Laura J Skinner, Simon C Satchell, Matthew J Butler

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. The renin angiotensin aldosterone system.Pflugers Archiv : European journal of physiology · 2024
    Review
  12. Review
  13. Review
  14. Renal tubular SGK1 is required to achieve blood pressure surge and circadian rhythm.American journal of physiology. Renal physiology · 2023
    Article
  15. 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

4 authors at 1 institution in 1 country.

Michael CromptonBristol Renal, Dorothy Hodgkin Building, University of Bristol, Whitson Street, Bristol BS1 3NY, UK.ORCID 0000-0001-6463-9020
Laura J SkinnerBristol Renal, Dorothy Hodgkin Building, University of Bristol, Whitson Street, Bristol BS1 3NY, UK.
Simon C SatchellBristol Renal, Dorothy Hodgkin Building, University of Bristol, Whitson Street, Bristol BS1 3NY, UK.
Matthew J ButlerBristol Renal, Dorothy Hodgkin Building, University of Bristol, Whitson Street, Bristol BS1 3NY, UK.
University of Bristol · GB

Funding

British Heart Foundation FS/CRTF/22/24361British Heart Foundation PG/20/10187Medical Research Council MR/M018237/1Medical Research Council MR/M018237/1/MRCMedical Research Council MR/T031921/1Medical Research Council MR/T031921/1/MRCMedical Research Council MR/W024187/1
6 · The paper itself

Abstract

The renin angiotensin aldosterone system is a key regulator of blood pressure. Aldosterone is the final effector of this pathway, acting predominantly via mineralocorticoid receptors. Aldosterone facilitates the conservation of sodium and, with it, water and acts as a powerful stimulus for potassium excretion. However, evidence for the pathological impact of excess mineralocorticoid receptor stimulation is increasing. Here, we discussed how in the heart, hyperaldosteronism is associated with fibrosis, cardiac dysfunction, and maladaptive hypertrophy. In the kidney, aldosterone was shown to cause proteinuria and fibrosis and may contribute to the progression of kidney disease. More recently, studies suggested that aldosterone excess damaged endothelial cells. Here, we reviewed how damage to the endothelial glycocalyx may contribute to this process. The endothelial glycocalyx is a heterogenous, negatively charged layer on the luminal surface of cells. Aldosterone exposure alters this layer. The resulting structural changes reduced endothelial reactivity in response to protective shear stress, altered permeability, and increased immune cell trafficking. Finally, we reviewed current therapeutic strategies for limiting endothelial damage and suggested that preventing glycocalyx remodelling in response to aldosterone exposure may provide a novel strategy, free from the serious adverse effect of hyperkalaemia seen in response to mineralocorticoid blockade.

Indexed as

AldosteroneEndothelium, VascularEndothelial CellsFibrosisHumansMineralocorticoid Receptor AntagonistsAldosteroneMineralocorticoid Receptor Antagonistsaldosteroneendotheliumglycocalyxmineralocorticoid receptor

Identifiers

PMID37371584
PMCPMC10296074
OpenAlexW4381252395

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.