Evidence map›Paper›PMID 28438162›Full record

ArticleRespiratory research2017

Targeting of nicotinamide phosphoribosyltransferase enzymatic activity ameliorates lung damage induced by ischemia/reperfusion in rats.

Geng-Chin Wu, Wen-I Liao, Shu-Yu Wu, Hsin-Ping Pao, Shih-En Tang, Min-Hui Li, Kun-Lun Huang, Shi-Jye Chu

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Intracellular NADJournal of cellular and molecular medicine · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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.

Geng-Chin WuThe Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.
Wen-I LiaoDepartment of Emergency Medicine, Tri-Service General Hospital, Taipei, Taiwan.
Shu-Yu WuThe Graduate Institute of Aerospace and Undersea Medicine, National Defense Medical Center, Taipei, Taiwan.
Hsin-Ping PaoThe Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.
Shih-En TangDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Tri-Service General Hospital, Taipei, Taiwan.
Min-Hui LiDepartment of Physical Medicine and Rehabilitation, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.
Kun-Lun HuangThe Graduate Institute of Aerospace and Undersea Medicine, National Defense Medical Center, Taipei, Taiwan. kun@mail.ndmctsgh.edu.tw.
Shi-Jye ChuDepartment of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Section 2, Chenggong Road, Neihu 114, Taipei, Taiwan. d1204812@mail.ndmctsgh.edu.tw.
National Defense Medical Center · TWTri-Service General Hospital · TWKaohsiung Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEmerging evidence reveals that nicotinamide phosphoribosyltransferase (NAMPT) has a significant role in the pathophysiology of the inflammatory process. NAMPT inhibition has a beneficial effect in the treatment of a variety of inflammatory diseases. However, it remains unclear whether NAMPT inhibition has an impact on ischemia-reperfusion (I/R)-induced acute lung injury. In this study, we examined whether NAMPT inhibition provided protection against I/R lung injury in rats.

methodsIsolated perfused rat lungs were subjected to 40 min of ischemia followed by 60 min of reperfusion. The rats were randomly allotted to the control, control + FK866 (NAMPT inhibitor, 10 mg/kg), I/R, or I/R + FK866 groups (n = 6 per group). The effects of FK866 on human alveolar epithelial cells exposed to hypoxia-reoxygenation (H/R) were also investigated.

resultsTreatment with FK866 significantly attenuated the increases in lung edema, pulmonary arterial pressure, lung injury scores, and TNF-α, CINC-1, and IL-6 concentrations in bronchoalveolar lavage fluid in the I/R group. Malondialdehyde levels, carbonyl contents and MPO-positive cells in lung tissue were also significantly reduced by FK866. Additionally, FK866 mitigated I/R-stimulated degradation of IκB-α, nuclear translocation of NF-κB, Akt phosphorylation, activation of mitogen-activated protein kinase, and downregulated MKP-1 activity in the injured lung tissue. Furthermore, FK866 increased Bcl-2 and decreased caspase-3 activity in the I/R rat lungs. Comparably, the in vitro experiments showed that FK866 also inhibited IL-8 production and NF-κB activation in human alveolar epithelial cells exposed to H/R.

conclusionsOur findings suggest that NAMPT inhibition may be a novel therapeutic approach for I/R-induced lung injury. The protective effects involve the suppression of multiple signal pathways.

Indexed as

AcrylamidesAcute Lung InjuryAnimalsCytokinesEnzyme ActivationLungMaleMolecular Targeted TherapyNicotinamide PhosphoribosyltransferasePiperidinesRatsRats, Sprague-DawleyReperfusion InjuryTreatment OutcomeAcrylamidesCytokinesN-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamideNicotinamide PhosphoribosyltransferasePiperidinesAcute lung injuryIschemia-reperfusionNicotinamide phosphoribosyltransferasepre-B cell colony-enhancing factorVisfatin

Identifiers

PMID28438162
PMCPMC5404693
OpenAlexW2607715547

What OpenQuestion holds

Textmetadata
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.