Evidence map›Paper›PMID 19495412›Full record

ArticlePloS one2009

Heme oxygenase-1 accelerates cutaneous wound healing in mice.

Anna Grochot-Przeczek, Radoslaw Lach, Jacek Mis, Klaudia Skrzypek, Malgorzata Gozdecka, Patrycja Sroczynska, Milena Dubiel, Andrzej Rutkowski, Magdalena Kozakowska, Anna Zagorska and 9 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

70 citing papers in PubMed, 128 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Current issues in molecular biology · 2024
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Heme Oxygenase-1 as Therapeutic Target for Diabetic Foot Ulcers.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. Article
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  16. Anti-inflammatory effects of haptoglobin on LPS-stimulated macrophages: Role of HMGB1 signaling and implications in chronic wound healing.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2020
    Article
  17. Article
  18. Review
  19. Article
  20. Article

10 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

19 authors at 4 institutions in 2 countries.

Anna Grochot-PrzeczekDepartment of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland.
Radoslaw Lach
Jacek Mis
Klaudia Skrzypek
Malgorzata Gozdecka
Patrycja Sroczynska
Milena Dubiel
Andrzej Rutkowski
Magdalena Kozakowska
Anna Zagorska
Jacek Walczynski
Halina Was
Jerzy Kotlinowski
Justyna Drukala
Krzysztof Kurowski
Claudine Kieda
Yann Herault
Jozef Dulak
Alicja Jozkowicz
Jagiellonian University · PLAdamed (Poland) · PLCentre National de la Recherche Scientifique · FRTransgene (France) · FR

Funding

Wellcome Trust
6 · The paper itself

Abstract

Heme oxygenase-1 (HO-1), a cytoprotective, pro-angiogenic and anti-inflammatory enzyme, is strongly induced in injured tissues. Our aim was to clarify its role in cutaneous wound healing. In wild type mice, maximal expression of HO-1 in the skin was observed on the 2(nd) and 3(rd) days after wounding. Inhibition of HO-1 by tin protoporphyrin-IX resulted in retardation of wound closure. Healing was also delayed in HO-1 deficient mice, where lack of HO-1 could lead to complete suppression of reepithelialization and to formation of extensive skin lesions, accompanied by impaired neovascularization. Experiments performed in transgenic mice bearing HO-1 under control of keratin 14 promoter showed that increased level of HO-1 in keratinocytes is enough to improve the neovascularization and hasten the closure of wounds. Importantly, induction of HO-1 in wounded skin was relatively weak and delayed in diabetic (db/db) mice, in which also angiogenesis and wound closure were impaired. In such animals local delivery of HO-1 transgene using adenoviral vectors accelerated the wound healing and increased the vascularization. In summary, induction of HO-1 is necessary for efficient wound closure and neovascularization. Impaired wound healing in diabetic mice may be associated with delayed HO-1 upregulation and can be improved by HO-1 gene transfer.

Indexed as

Wound HealingAdenoviridaeAngiogenesis InhibitorsAnimalsAnti-Inflammatory AgentsDiabetes Mellitus, ExperimentalGene Transfer TechniquesHeme Oxygenase-1HumansInflammationKeratinsMiceMice, Inbred C57BLPromoter Regions, GeneticTransgenesAngiogenesis InhibitorsAnti-Inflammatory AgentsHeme Oxygenase-1Keratins

Identifiers

PMID19495412
PMCPMC2686151
OpenAlexW2135022152

What OpenQuestion holds

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LicenceCC BY
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.