Evidence map›Paper›PMID 24691203›Full record

ArticlePloS one2014

New perspectives in the renin-angiotensin-aldosterone system (RAAS) II: albumin suppresses angiotensin converting enzyme (ACE) activity in human.

Miklós Fagyas, Katalin Úri, Ivetta M Siket, Gábor Á Fülöp, Viktória Csató, Andrea Daragó, Judit Boczán, Emese Bányai, István Elek Szentkirályi, Tamás Miklós Maros and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Albumin Is an Integrative Protein of Blood Plasma and Beyond.International journal of molecular sciences · 2024
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Peptide derivedHeliyon · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. 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

14 authors at 1 institution in 1 country.

Miklós FagyasDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary.
Katalin ÚriDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary.
Ivetta M SiketDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary.
Gábor Á FülöpDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary.
Viktória CsatóDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary.
Andrea DaragóDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary.
Judit BoczánDepartment of Neurology, University of Debrecen, Debrecen, Hungary.
Emese BányaiInstitute of Internal Medicine, Division of Nephrology, University of Debrecen, Debrecen, Hungary.
István Elek SzentkirályiDepartment of Cardiac Surgery, Institute of Cardiology, University of Debrecen, Debrecen, Hungary.
Tamás Miklós MarosDepartment of Cardiac Surgery, Institute of Cardiology, University of Debrecen, Debrecen, Hungary.
Tamás SzerafinDepartment of Cardiac Surgery, Institute of Cardiology, University of Debrecen, Debrecen, Hungary.
István ÉdesDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary.
Zoltán PappDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary.
Attila TóthDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary.
University of Debrecen · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

About 8% of the adult population is taking angiotensin-converting enzyme (ACE) inhibitors to treat cardiovascular disease including hypertension, myocardial infarction and heart failure. These drugs decrease mortality by up to one-fifth in these patients. We and others have reported previously that endogenous inhibitory substances suppress serum ACE activity, in vivo, similarly to the ACE inhibitor drugs. Here we have made an effort to identify this endogenous ACE inhibitor substance. ACE was crosslinked with interacting proteins in human sera. The crosslinked products were immunoprecipitated and subjected to Western blot. One of the crosslinked products was recognized by both anti-ACE and anti-HSA (human serum albumin) antibodies. Direct ACE-HSA interaction was confirmed by binding assays using purified ACE and HSA. HSA inhibited human purified (circulating) and human recombinant ACE with potencies (IC50) of 5.7 ± 0.7 and 9.5 ± 1.1 mg/mL, respectively. Effects of HSA on the tissue bound native ACE were tested on human saphenous vein samples. Angiotensin I evoked vasoconstriction was inhibited by HSA in this vascular tissue (maximal force with HSA: 6.14 ± 1.34 mN, without HSA: 13.54 ± 2.63 mN), while HSA was without effects on angiotensin II mediated constrictions (maximal force with HSA: 18.73 ± 2.17 mN, without HSA: 19.22 ± 3.50 mN). The main finding of this study is that HSA was identified as a potent physiological inhibitor of the ACE. The enzymatic activity of ACE appears to be almost completely suppressed by HSA when it is present in its physiological concentration. These data suggest that angiotensin I conversion is limited by low physiological ACE activities, in vivo.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAngiotensin IBiomechanical PhenomenaCatalytic DomainHumansKineticsMolecular WeightPeptidyl-Dipeptidase ARecombinant ProteinsRenin-Angiotensin SystemSaphenous VeinSerum AlbuminACE protein, humanAngiotensin-Converting Enzyme InhibitorsAngiotensin IPeptidyl-Dipeptidase ARecombinant ProteinsSerum Albumin

Identifiers

PMID24691203
PMCPMC3972182
OpenAlexW2070148485

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.