Evidence map›Paper›PMID 25781495›Full record

ArticleJournal of cellular and molecular medicine2015

Renalase contributes to the renal protection of delayed ischaemic preconditioning via the regulation of hypoxia-inducible factor-1α.

Feng Wang, Guangyuan Zhang, Tao Xing, Zeyuan Lu, Junhui Li, Cheng Peng, Guohua Liu, Niansong Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.3field-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

25 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Renalase: a novel regulator of cardiometabolic and renal diseases.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Extracellular renalase protects cells and organs by outside-in signalling.Journal of cellular and molecular medicine · 2017
    Review
  19. Article
  20. Clinical science (London, England : 1979) · 2017
    Review
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 4 institutions in 2 countries.

Feng WangDepartment of Nephrology and Rheumatology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Guangyuan ZhangDepartment of Urology, Shanghai Jiao Tong University Affiliated First People's Hospital, Shanghai, China.
Tao XingSt. Vincent's Hospital, Melbourne, VIC, Australia.
Zeyuan LuDepartment of Nephrology and Rheumatology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Junhui LiDepartment of Nephrology and Rheumatology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Cheng PengDepartment of Nephrology and Rheumatology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Guohua LiuDepartment of Urology, Shanghai Jiao Tong University Affiliated First People's Hospital, Shanghai, China.
Niansong WangDepartment of Nephrology and Rheumatology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Shanghai Jiao Tong University · CNShanghai First People's Hospital · CNShanghai Sixth People's Hospital · CNSt Vincent's Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischaemic preconditioning (IPC) attenuates acute kidney injury (AKI) from renal ischaemia reperfusion. Renalase, an amine oxidase secreted by the proximal tubule, not only degrades circulating catecholamines but also protects against renal ischaemia reperfusion injury. Here, it has been suggested that the renoprotective effect of renal IPC is partly mediated by renalase. In a model of brief intermittent renal IPC, the increased cortex renalase expression was found to last for 48 hrs. IPC significantly reduced renal tubular inflammation, necrosis and oxidative stress following renal ischaemia reperfusion injury. Such effects were attenuated by blocking renalase with an anti-renalase monoclonal antibody. We further demonstrated that renalase expression was up-regulated by hypoxia in vitro via an hypoxia-inducible factor (HIF)-1α mechanism. The IPC-induced up-regulation of renalase in vivo was also reduced by pre-treatment with an HIF-1α inhibitor, 3-(5'-Hydroxymethyl-2'-furyl)-1-benzyl indazole. In summary, the renoprotective effect of IPC is partly dependent on the renalase expression, which may be triggered by hypoxia via an HIF-1α mechanism. Endogenous renalase shows potential as a therapeutic agent for the prevention and treatment of AKI.

Indexed as

Ischemic PreconditioningAnimalsBlotting, WesternCell HypoxiaCell LineGene Expression Regulation, EnzymologicHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitKidneyMaleMonoamine OxidaseProtective AgentsRats, Sprague-DawleyReperfusion InjuryReverse Transcriptase Polymerase Chain ReactionHypoxia-Inducible Factor 1, alpha SubunitMonoamine OxidaseProtective Agentsrenalasehypoxia-inducible factorischaemia/reperfusion injuryischaemic preconditioningrenalase

Identifiers

PMID25781495
PMCPMC4459853
OpenAlexW1996440251

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.