Evidence map›Paper›PMID 24275768›Full record

ReviewCurrent opinion in nephrology and hypertension2014

Heme oxygenase-1 and acute kidney injury.

Karl A Nath

Abstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

75 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Targeting ferroptosis in ischemia/reperfusion renal injury.Naunyn-Schmiedeberg's archives of pharmacology · 2022
    Review
  13. Review
  14. Article
  15. Review
  16. The spike protein of SARS-CoV-2 induces heme oxygenase-1: Pathophysiologic implications.Biochimica et biophysica acta. Molecular basis of disease · 2022
    Article
  17. Review
  18. Article
  19. Article
  20. Review

15 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Karl A NathaDivision of Nephrology and Hypertension, Department of Medicine bDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.
Mayo Clinic · US

Funding

Renal Injury and Adaptation to Heme ProteinsR37DK047060 · NIDDK · MAYO CLINIC ROCHESTER · PI NATH, KARL A. · 2002 to 2011
$3.6M
Mechanism of Dialysis Arteriovenous Fistula DysfunctionR01DK070124 · NIDDK · MAYO CLINIC ROCHESTER · PI NATH, KARL A. · 2005 to 2015
$3.4M
RENAL INJURY AND ADAPTATION TO HEME PROTEINSR01DK047060 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI NATH, KARL A. · 1993 to 2018
$2.2M
NIDDK NIH HHS DK47060NIDDK NIH HHS DK70124NIDDK NIH HHS R01 DK047060NIDDK NIH HHS R01 DK070124NIDDK NIH HHS R37 DK047060
6 · The paper itself

Abstract

purpose of reviewHeme oxygenase activity, possessed by an inducible heme oxygenase-1 (HO-1) and a constitutive isoform (HO-2), catalyzes the conversion of heme to biliverdin, liberates iron, and generates carbon monoxide. First shown in acute kidney injury (AKI), HO-1 is now recognized as a protectant against diverse insults in assorted tissues. This review summarizes recent contributions to the field of HO-1 and AKI. RECENT

findingsRecent findings elucidate the following: the transcriptional regulation and significance of human HO-1 in AKI; the protective effects of HO-1 in age-dependent and sepsis-related AKI, cardiorenal syndromes, and acute vascular rejection in renal xenografts; the role of heme oxygenase in tubuloglomerular feedback and renal resistance to injury; the basis for cytoprotection by HO-1; the protective properties of ferritin and carbon monoxide; HO-1 and the AKI-chronic kidney disease transition; HO-1 as a biomarker in AKI; the role of HO-1 in mediating the protective effects of specific cytokines, stem cells, and therapeutic agents in AKI; and HO-2 as a protectant in AKI. SUMMARY: Recent contributions support, and elucidate the basis for, the induction of HO-1 as a protectant against AKI. Translating such therapeutic potential into a therapeutic reality requires well tolerated and effective modalities for upregulating HO-1 and/or administering its products, which, optimally, should be salutary even when AKI is already established.

Indexed as

Acute Kidney InjuryAnimalsDisease Models, AnimalHeme Oxygenase-1HumansKidneyPrognosisRisk FactorsSignal TransductionHeme Oxygenase-1

Identifiers

PMID24275768
PMCPMC4137976
OpenAlexW2068825117

What OpenQuestion holds

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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.