Evidence map›Paper›PMID 16816358›Full record

ArticleThe American journal of pathology2006

Anomalous renal effects of tin protoporphyrin in a murine model of sickle cell disease.

Julio P Juncos, Joseph P Grande, Narayana Murali, Anthony J Croatt, Luis A Juncos, Robert P Hebbel, Zvonimir S Katusic, Karl A Nath

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases.International journal of molecular sciences · 2021
    Review
  5. Review
  6. Article
  7. Marked protection against acute renal and hepatic injury after nitrited myoglobin + tin protoporphyrin administration.Translational research : the journal of laboratory and clinical medicine · 2015
    Article
  8. Article
  9. Induction and functional significance of the heme oxygenase system in pathological shear stress in vivo.American journal of physiology. Heart and circulatory physiology · 2015
    Article
  10. Article
  11. Article
  12. Genetic deficiency of Smad3 protects against murine ischemic acute kidney injury.American journal of physiology. Renal physiology · 2011
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

8 authors at 3 institutions in 1 country.

Julio P JuncosDivision of Nephrology and Hypertension, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.
Joseph P Grande
Narayana Murali
Anthony J Croatt
Luis A Juncos
Robert P Hebbel
Zvonimir S Katusic
Karl A Nath
Mayo Clinic · USTherapeutics Clinical Research · USUniversity of Minnesota Medical Center · US

Funding

VASCULAR PATHOBIOLOGY OF SICKLE CELL DISEASEP01HL055552 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI HEBBEL, ROBERT P · 1995 to 2011
$17.3M
Renal Injury and Adaptation to Heme ProteinsR37DK047060 · NIDDK · MAYO CLINIC ROCHESTER · PI NATH, KARL A. · 2002 to 2011
$3.6M
RENAL INJURY AND ADAPTATION TO HEME PROTEINSR01DK047060 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI NATH, KARL A. · 1993 to 2018
$2.2M
NHLBI NIH HHS HL-55552NHLBI NIH HHS P01 HL055552NIDDK NIH HHS DK 47060NIDDK NIH HHS R01 DK047060NIDDK NIH HHS R37 DK047060
6 · The paper itself

Abstract

In human and murine models of sickle cell disease (SCD), heme oxygenase-1 (HO-1) is induced in the kidney, an organ commonly involved in SCD. The present study assessed the role of HO-1 by using a competitive inhibitor of HO activity, tin protoporphyrin (SnPP), in protocols affording a composite, clinically relevant analysis of the kidney in SCD under unstressed and stressed conditions. Whereas short-term administration of SnPP exerted comparable renal hemodynamic effects in wild-type and sickle mice, chronic administration of SnPP exerted divergent effects: SnPP provoked tubulointerstitial inflammation and up-regulation of injury-related genes in wild-type mice, whereas in sickle mice SnPP reduced expression of injury-related genes and vascular congestion without provoking tubulointerstitial inflammation. SnPP also protected against the heightened sensitivity to renal ischemia observed in sickle mice, preventing ischemia-induced worsening of renal injury in sickle mice above that observed in wild-type mice. Effective and comparable inhibition of HO activity by SnPP in wild-type and sickle mice was confirmed. These findings suggest that induction of HO-1, at least as assessed by this approach, may contribute to renal injury in this murine model of SCD and uncover an experimental maneuver that protects the kidney in murine SCD.

Indexed as

AnimalsDisease Models, AnimalDogsFemaleHeme Oxygenase-1Hemoglobin SC DiseaseKidneyKidney DiseasesKidney Function TestsMaleMetalloporphyrinsMiceMice, TransgenicProtoporphyrinsReperfusion InjuryReverse Transcriptase Polymerase Chain ReactionHeme Oxygenase-1MetalloporphyrinsProtoporphyrinsRNA, Messengertin protoporphyrin IX

Identifiers

PMID16816358
PMCPMC1698751
OpenAlexW2033507768

What OpenQuestion holds

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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.