Evidence map›Paper›PMID 17589825›Full record

ArticleDiabetologia2007

Anti-inflammatory effects of atorvastatin improve left ventricular function in experimental diabetic cardiomyopathy.

S Van Linthout, A Riad, N Dhayat, F Spillmann, J Du, S Dhayat, D Westermann, D Hilfiker-Kleiner, M Noutsias, U Laufs and 2 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

56 citing papers in PubMed, 127 citations in OpenAlex.

  1. Review
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  8. Article
  9. Review
  10. Diabetic fibrosis.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Review
  11. Review
  12. Article
  13. New Targets in Heart Failure Drug Therapy.Frontiers in cardiovascular medicine · 2021
    Review
  14. The potential of Atorvastatin for chronic lung diseases therapy.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2020
    Review
  15. Article
  16. Article
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  18. Article
  19. 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

12 authors at 3 institutions in 1 country.

S Van LinthoutDepartment of Cardiology and Pneumology, Campus Benjamin Franklin, Charité-University Medicine Berlin, Hindenburgdamm 30, 12200, Berlin, Germany.
A RiadDepartment of Cardiology and Pneumology, Campus Benjamin Franklin, Charité-University Medicine Berlin, Hindenburgdamm 30, 12200, Berlin, Germany.
N DhayatDepartment of Cardiology and Pneumology, Campus Benjamin Franklin, Charité-University Medicine Berlin, Hindenburgdamm 30, 12200, Berlin, Germany.
F SpillmannDepartment of Cardiology and Pneumology, Campus Benjamin Franklin, Charité-University Medicine Berlin, Hindenburgdamm 30, 12200, Berlin, Germany.
J DuDepartment of Cardiology and Pneumology, Campus Benjamin Franklin, Charité-University Medicine Berlin, Hindenburgdamm 30, 12200, Berlin, Germany.
S DhayatDepartment of Cardiology and Pneumology, Campus Benjamin Franklin, Charité-University Medicine Berlin, Hindenburgdamm 30, 12200, Berlin, Germany.
D WestermannDepartment of Cardiology and Pneumology, Campus Benjamin Franklin, Charité-University Medicine Berlin, Hindenburgdamm 30, 12200, Berlin, Germany.
D Hilfiker-KleinerDepartment of Cardiology, Medical School Hannover, Hannover, Germany.
M NoutsiasDepartment of Cardiology and Pneumology, Campus Benjamin Franklin, Charité-University Medicine Berlin, Hindenburgdamm 30, 12200, Berlin, Germany.
U LaufsDepartment of Cardiology, University of Saarland, Homburg/Saar, Germany.
H-P SchultheissDepartment of Cardiology and Pneumology, Campus Benjamin Franklin, Charité-University Medicine Berlin, Hindenburgdamm 30, 12200, Berlin, Germany.
C TschöpeDepartment of Cardiology and Pneumology, Campus Benjamin Franklin, Charité-University Medicine Berlin, Hindenburgdamm 30, 12200, Berlin, Germany. ctschoepe@yahoo.com.
Charité - Universitätsmedizin Berlin · DEMedizinische Hochschule Hannover · DESaarland University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisEmerging evidence suggests that statins exert beneficial effects beyond those predicted by their cholesterol-lowering actions. We investigated whether atorvastatin influences the development of left ventricular (LV) dysfunction, independently of cholesterol-lowering, in an experimental model of type 1 diabetes mellitus cardiomyopathy.

methodsStreptozotocin-induced diabetic rats were treated with atorvastatin (50 mg/kg daily, orally) or with vehicle for 6 weeks. LV function was analysed using tip-catheter measurements. Cardiac stainings of TNF-alpha, IL-1beta, intercellular adhesion molecule-1, vascular cellular adhesion molecule-1, CD11a/lymphocyte-associated antigen-1, CD11b/macrophage antigen alpha, CD18/beta2-integrin, ED1/CD68, collagen I and III, and Sirius Red were assessed by digital image analysis. Ras-related C3 botulinum toxin substrate (RAC1) and ras homologue gene family, member A (RHOA) activities were determined by RAC1 glutathione-S-transferase-p21-activated kinase and rhotekin pull-down assays, respectively. Cardiac lipid peroxides were measured by a colorimetric assay. The phosphorylation state of p38 mitogen-activated protein kinase (MAPK) and endothelial nitric oxide synthase (eNOS) protein production were analysed by western blot.

resultsDiabetes was associated with induced cardiac stainings of TNF-alpha, IL-1beta, cellular adhesion molecules, increased leucocyte infiltration, macrophage residence and cardiac collagen content. In contrast, atorvastatin reduced both intramyocardial inflammation and myocardial fibrosis, resulting in improved LV function. This effect was paralleled with a normalisation of diabetes-induced RAC1 and RHOA activity, in the absence of LDL-cholesterol lowering. In addition, atorvastatin decreased diabetes-induced cardiac lipid peroxide levels and p38 MAPK phosphorylation by 1.3-fold (p < 0.05) and 3.2-fold (p < 0.0005), respectively, and normalised the reduced eNOS production caused by diabetes. CONCLUSIONS/

interpretationThese data indicate that atorvastatin, independently of its LDL-cholesterol-lowering capacity, reduces intramyocardial inflammation and myocardial fibrosis, resulting in improved LV function in an experimental model of diabetic cardiomyopathy.

Indexed as

AnimalsAnti-Inflammatory AgentsAtorvastatinCollagenDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetic AngiopathiesHeartHeptanoic AcidsInflammationMyocardiumPyrrolesRatsRats, Sprague-DawleyVentricular Dysfunction, LeftVentricular Function, LeftAnti-Inflammatory AgentsAtorvastatinCollagenHeptanoic AcidsPyrroles

Identifiers

PMID17589825
OpenAlexW1976161092

What OpenQuestion holds

Textmetadata
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.