Evidence map›Paper›PMID 25096529›Full record

ArticleCritical care (London, England)2014

Silencing airway epithelial cell-derived hepcidin exacerbates sepsis induced acute lung injury.

Qi Xing Chen, Sheng Wen Song, Qing Hua Chen, Cong Li Zeng, Xia Zheng, Jun Lu Wang, Xiang Ming Fang

Open access · goldAbstract read
In one paragraph

Article in Critical care (London, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

  1. Iron and the lung: emerging roles of iron metabolism in pulmonary disease pathogenesis and therapy.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  2. Article
  3. Review
  4. Hepcidin and Tissue-Specific Iron Regulatory Networks.Advances in experimental medicine and biology · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Apelin/APJ system: an emerging therapeutic target for respiratory diseases.Cellular and molecular life sciences : CMLS · 2020
    Review
  9. Article
  10. Review
  11. Iron in Lung Pathology.Pharmaceuticals (Basel, Switzerland) · 2019
    Review
  12. Review
  13. Balance of cardiac and systemic hepcidin and its role in heart physiology and pathology.Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  14. Article
  15. Article
  16. Review
  17. Iron is essential for living!Critical care (London, England) · 2014
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Qi Xing Chen
Sheng Wen Song
Qing Hua Chen
Cong Li Zeng
Xia Zheng
Jun Lu Wang
Xiang Ming Fang
Zhejiang University · CNFirst Affiliated Hospital of Wenzhou Medical University · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe production of antimicrobial peptides by airway epithelial cells is an important component of the innate immune response to pulmonary infection and inflammation. Hepcidin is a β-defensin-like antimicrobial peptide and acts as a principal iron regulatory hormone. Hepcidin is mostly produced by hepatocytes, but is also expressed by other cells, such as airway epithelial cells. However, nothing is known about its function in lung infectious and inflammatory diseases. We therefore sought to investigate the role of airway epithelial cell-derived hepcidin in sepsis-induced acute lung injury.

methodsAcute lung injury was induced by polymicrobial sepsis via cecal ligation and puncture (CLP) surgery. Adenovirus-mediated short hairpin RNA specific for the mouse hepcidin gene hepc1 and control adenovirus were intratracheally injected into mice. The adenovirus-mediated knockdown of hepcidin in airway epithelial cells was evaluated in vivo. Lung injury and the 7-day survival rate were assessed. The levels of hepcidin-related iron export protein ferroportin were measured, and the iron content and function of alveolar macrophages were evaluated.

resultsThe hepcidin level in airway epithelial cells was upregulated during polymicrobial sepsis. The knockdown of airway epithelial cell-derived hepcidin aggravated the polymicrobial sepsis-induced lung injury and pulmonary bacterial infection and increased the mortality (53.33% in Ad-shHepc1 treated mice versus 12.5% in Ad-shNeg treated mice, P <0.05). The knockdown of hepcidin in airway epithelial cells also led to reduced ferroportin degradation and a low intracellular iron content in alveolar macrophages. Moreover, alveolar macrophages form the airway epithelial cell-derived hepcidin knockdown mice showed impaired phagocytic ability than those from the control mice.

conclusionsAirway epithelial cell-derived hepcidin plays an important role in CLP induced acute lung injury. The severe lung injury in the airway epithelial cell-derived hepcidin knockdown mice is at least partially related to the altered intracellular iron level and function of alveolar macrophages.

Indexed as

Acute Lung InjuryAnimalsBronchoalveolar Lavage FluidCoinfectionColony Count, MicrobialDisease Models, AnimalDisease ProgressionEpithelial CellsHepcidinsImmunohistochemistryIronMaleMiceMice, Inbred C57BLRespiratory SystemSepsisHepcidinsIron

Identifiers

PMID25096529
PMCPMC4243715
OpenAlexW2137800298

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.