Evidence map›Paper›PMID 23116220›Full record

ArticleClinical science (London, England : 1979)2013

Direct renin inhibition prevents cardiac dysfunction in a diabetic mouse model: comparison with an angiotensin receptor antagonist and angiotensin-converting enzyme inhibitor.

Candice M Thomas, Qian Chen Yong, Rachid Seqqat, Niketa Chandel, David L Feldman, Kenneth M Baker, Rajesh Kumar

Abstract readComparative Study
In one paragraph

Article in Clinical science (London, England : 1979), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Metabolites · 2022
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Renin Activity in Heart Failure with Reduced Systolic Function-New Insights.International journal of molecular sciences · 2019
    Review
  15. Article
  16. Review
  17. Diabetic cardiomyopathy: where we are and where we are going.The Korean journal of internal medicine · 2017
    Review
  18. Article
  19. Article
  20. Structure and functions of angiotensinogen.Hypertension research : official journal of the Japanese Society of Hypertension · 2016
    Review
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 1 institution in 2 countries.

Candice M ThomasDivision of Molecular Cardiology, Department of Medicine, Texas A&M Health Science Center, College of Medicine; Scott and White; Central Texas Veterans Health Care System, Temple, TX 76504, USA.
Qian Chen Yong
Rachid Seqqat
Niketa Chandel
David L Feldman
Kenneth M Baker
Rajesh Kumar
Baylor Scott & White Health · US

Funding

Novel Aspects of the Cardiac Renin-Angiotensin SystemR01HL090817 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI BAKER, KENNETH MELVIN · 2009 to 2012
$1.3M
NHLBI NIH HHS 5R01HL090817NHLBI NIH HHS R01 HL090817
6 · The paper itself

Abstract

Hyperglycaemia up-regulates intracellular AngII (angiotensin II) production in cardiac myocytes, effects of which are blocked more effectively by renin inhibition than ARBs (angiotensin receptor blockers) or ACEis (angiotensin-converting enzyme inhibitors). In the present study, we determined whether renin inhibition is more effective at preventing diabetic cardiomyopathy than an ARB or ACEi. Diabetes was induced in adult mice for 10 weeks by STZ (streptozotocin). Diabetic mice were treated with insulin, aliskiren (a renin inhibitor), benazeprilat (an ACEi) or valsartan (an ARB) via subcutaneous mini-pumps. Significant impairment in diastolic and systolic cardiac functions was observed in diabetic mice, which was completely prevented by all three RAS (renin-angiotensin system) inhibitors. Hyperglycaemia significantly increased cardiac oxidative stress and circulating inflammatory cytokines, which were blocked by aliskiren and benazeprilat, whereas valsartan was partially effective. Diabetes increased cardiac PRR (prorenin receptor) expression and nuclear translocation of PLZF (promyelocytic zinc finger protein), which was completely prevented by aliskiren and valsartan, and partially by benazeprilat. Renin inhibition provided similar protection of cardiac function to ARBs and ACEis. Activation of PLZF by PRR represented a novel mechanism in diabetic cardiomyopathy. Differential effects of the three agents on oxidative stress, cytokines and PRR expression suggested subtle differences in their mechanisms of action.

Indexed as

Renin InhibitorsAmidesAngiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsAnimalsBenzazepinesBlood PressureDiabetes Mellitus, ExperimentalFumaratesHeartHumansMaleMiceMice, Inbred C57BLMyocardiumOxidative StressaliskirenAmidesAngiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsbenazeprilatBenzazepinesFumaratesProrenin ReceptorReceptors, Cell SurfaceReninRenin InhibitorsTetrazolesValineValsartan

Identifiers

PMID23116220
PMCPMC3982397
OpenAlexW2033192281

What OpenQuestion holds

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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.