Evidence map›Paper›PMID 18463318›Full record

ArticleAmerican journal of physiology. Renal physiology2008

Renoprotection by statins is linked to a decrease in renal oxidative stress, TGF-beta, and fibronectin with concomitant increase in nitric oxide bioavailability.

Ming-Sheng Zhou, Ivonne Hernandez Schuman, Edgar A Jaimes, Leopoldo Raij

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 6% 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, 2 syntheses or guidelines pooled it, 96 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Oxidative Stress in Kidney Injury and Hypertension.Antioxidants (Basel, Switzerland) · 2024
    Review
  7. Article
  8. Observational
  9. Review
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  12. Review
  13. Article
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  17. Observational
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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

4 authors at 1 institution in 1 country.

Ming-Sheng ZhouNephrology-Hypertension Section, Veterans Affairs Medical Center, Vascular Biology Institute, University of Miami Miller School of Medicine, Miami, FL 33125, USA. mzhou2@med.miami.edu
Ivonne Hernandez Schuman
Edgar A Jaimes
Leopoldo Raij
University of Miami · US

Funding

Glomerular COX-2 in Hypertensive Renal DiseaseR03DK069372 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI JAIMES, EDGAR A · 2005 to 2007
$443k
NIDDK NIH HHS DK-069372
6 · The paper itself

Abstract

Clinical and experimental studies have provided evidence suggesting that statins exert renoprotective effects. To investigate the mechanisms by which statins may exert renoprotection, we utilized the hypertensive Dahl salt-sensitive (DS) rat model, which manifests cardiovascular and renal injury linked to increased angiotensin II-dependent activation of NADPH oxidase and decreased nitric oxide (NO) bioavailability. DS rats given high salt diet (4% NaCl) for 10 wk exhibited hypertension [systolic blood pressure (SBP) 200 +/- 8 vs. 150 +/- 2 mmHg in normal salt diet (0.5% NaCl), P < 0.05], glomerulosclerosis, and proteinuria (158%). This was associated with increased renal oxidative stress demonstrated by urinary 8-F(2alpha)-isoprostane excretion and NADPH oxidase activity, increased protein expression of transforming growth factor (TGF)-beta (63%) and fibronectin (181%), increased mRNA expression of the proinflammatory molecules monocyte chemoattractant protein-1 (MCP-1) and lectin-like oxidized LDL receptor-1 (LOX-1), as well as downregulation of endothelial NO synthase (eNOS) activity (-44%) and protein expression. Return to normal salt had no effect on SBP or any of the measured parameters. Atorvastatin (30 mg.kg(-1).day(-1)) significantly attenuated proteinuria and glomerulosclerosis and normalized renal oxidative stress, TGF-beta1, fibronectin, MCP-1 and LOX-1 expression, and eNOS activity and expression. Atorvastatin-treated rats showed a modest reduction in SBP that remained in the hypertensive range (174 +/- 8 mmHg). Atorvastatin combined with removal of high salt normalized SBP and proteinuria. These findings suggest that statins mitigate hypertensive renal injury by restoring the balance among NO, TGF-beta1, and oxidative stress and explain the added renoprotective effects observed in clinical studies using statins in addition to inhibitors of the renin-angiotensin system.

Indexed as

AnimalsAtorvastatinBiological AvailabilityBlood PressureChemokine CCL2FibronectinsHeptanoic AcidsHydroxymethylglutaryl-CoA Reductase InhibitorsKidneyKidney Failure, ChronicNADPH OxidasesNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIOxidative StressProteinuriaAtorvastatinCcl2 protein, ratChemokine CCL2FibronectinsHeptanoic AcidsHydroxymethylglutaryl-CoA Reductase InhibitorsNADPH OxidasesNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINos3 protein, ratPyrrolesRNA, MessengerScavenger Receptors, Class ETransforming Growth Factor beta

Identifiers

PMID18463318
PMCPMC2494511
OpenAlexW2126644100

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.