Evidence map›Paper›PMID 18495963›Full record

ArticleJournal of the American Society of Nephrology : JASN2008

Heme oxygenase-1 deficiency promotes epithelial-mesenchymal transition and renal fibrosis.

Jeong-Hae Kie, Matthias H Kapturczak, Amie Traylor, Anupam Agarwal, Nathalie Hill-Kapturczak

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

55 citing papers in PubMed, 87 citations in OpenAlex.

  1. Review
  2. Review
  3. The Triple Crown: NO, CO, and HPharmacology & therapeutics · 2023
    Review
  4. Review
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  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Expression of lactate dehydrogenase A and B isoforms in the mouse kidney.American journal of physiology. Renal physiology · 2021
    Article
  12. Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases.International journal of molecular sciences · 2021
    Review
  13. Review
  14. The Cross-Link between Ferroptosis and Kidney Diseases.Oxidative medicine and cellular longevity · 2021
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Jeong-Hae KieDepartment of Medicine, Division of Nephrology, Nephrology Research and Training Center, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
Matthias H Kapturczak
Amie Traylor
Anupam Agarwal
Nathalie Hill-Kapturczak
University of Alabama at Birmingham · USPediatric Nephrology of Alabama · US

Funding

Human Heme Oxygenase-1 Gene Regulation in Renal InjuryR01DK059600 · NIDDK · UNIVERSITY OF FLORIDA · PI AGARWAL, ANUPAM, GEORGE, JAMES F · 2002 to 2019
$4.5M
ARTERIAL ENDOTHELIAL FUNCTION--AN EPIDEMIOLOGIC STUDYR37HL061857 · NHLBI · UNIVERSITY OF IOWA · PI LAUER, RONALD M · 1999 to 2004
$3.5M
ARTERIAL ENDOTHELIAL FUNCTION--AN EPIDEMIOLOGIC STUDYR01HL061857 · NHLBI · UNIVERSITY OF IOWA · PI BURNS, TRUDY L · 2005 to 2008
$3.0M
Heme Oxygenase-1 Gene Expression by TGF-Beta1R01DK071875 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AGARWAL, ANUPAM · 2006 to 2008
$638k
NHLBI NIH HHS R01 HL061857NHLBI NIH HHS R37 HL061857NIDDK NIH HHS R01 DK059600NIDDK NIH HHS R01 DK071875NIDDK NIH HHS R01 DK59600
6 · The paper itself

Abstract

Induction of heme oxygenase-1 (HO-1) is associated with potential antifibrogenic effects. The effects of HO-1 expression on epithelial-mesenchymal transition (EMT), which plays a critical role in the development of renal fibrosis, are unknown. In this study, HO-1(-/-) mice demonstrated significantly more fibrosis after 7 d of unilateral ureteral obstruction compared with wild-type mice, despite similar degrees of hydronephrosis. The obstructed kidneys of HO-1(-/-) mice also had greater macrophage infiltration and renal tubular TGF-beta1 expression than wild-type mice. In addition, the degree of EMT was more extensive in obstructed HO-1(-/-) kidneys, as assessed by alpha-smooth muscle actin and expression of S100A4 in proximal tubular epithelial cells. In vitro studies using proximal tubular cells isolated from HO-1(-/-) and wild-type kidneys confirmed these observations. In conclusion, HO-1 deficiency is associated with increased fibrosis, tubular TGF-beta1 expression, inflammation, and enhanced EMT in obstructive kidney disease. Modulation of the HO-1 pathway may provide a new therapeutic approach to progressive renal diseases.

Indexed as

AnimalsBiomarkersCells, CulturedCell TransdifferentiationFibrosisHeme Oxygenase-1KidneyKidney Tubules, ProximalMacrophagesMiceMice, Inbred C57BLMice, KnockoutNephrosclerosisTransforming Growth Factor beta1Ureteral ObstructionBiomarkersHeme Oxygenase-1Transforming Growth Factor beta1

Identifiers

PMID18495963
PMCPMC2518436
OpenAlexW2149900560

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.