Evidence map›Paper›PMID 28049526›Full record

ArticleRespiratory research2017

Atrial natriuretic peptide protects against bleomycin-induced pulmonary fibrosis via vascular endothelial cells in mice : ANP for pulmonary fibrosis.

Atsuko Okamoto, Takashi Nojiri, Kazuhisa Konishi, Takeshi Tokudome, Koichi Miura, Hiroshi Hosoda, Jun Hino, Mikiya Miyazato, Yohkoh Kyomoto, Kazuhisa Asai and 2 more

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
2.7field-weighted citation impact, top 10% 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, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. The Vasculature in Pulmonary Fibrosis.Current tissue microenvironment reports · 2022
    Article
  6. Review
  7. Article
  8. Pseudomonas aeruginosa Biofilm Dispersion by the Human Atrial Natriuretic Peptide.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Article
  9. Article
  10. [Role of interleukin-6 in human umbilical vein endothelial cell to mesenchymal cell transformation].Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Meeting report of the 8Naunyn-Schmiedeberg's archives of pharmacology · 2017
    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

12 authors at 2 institutions in 1 country.

Atsuko OkamotoDepartment of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, 5-7-1, Fujishirodai, Suita-City, Osaka, 565-8565, Japan.
Takashi NojiriDepartment of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, 5-7-1, Fujishirodai, Suita-City, Osaka, 565-8565, Japan. nojiri@ri.ncvc.go.jp.
Kazuhisa KonishiDepartment of Respiratory Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka-City, Osaka, 545-8585, Japan. kkonishi.0220@gmail.com.
Takeshi TokudomeDepartment of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, 5-7-1, Fujishirodai, Suita-City, Osaka, 565-8565, Japan.
Koichi MiuraDepartment of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, 5-7-1, Fujishirodai, Suita-City, Osaka, 565-8565, Japan.
Hiroshi HosodaDepartment of Regenerative Medicine and Tissue Engineering, National Cerebral and Cardiovascular Center Research Institute, Suita-City, Osaka, Japan.
Jun HinoDepartment of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, 5-7-1, Fujishirodai, Suita-City, Osaka, 565-8565, Japan.
Mikiya MiyazatoDepartment of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, 5-7-1, Fujishirodai, Suita-City, Osaka, 565-8565, Japan.
Yohkoh KyomotoDepartment of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, 5-7-1, Fujishirodai, Suita-City, Osaka, 565-8565, Japan.
Kazuhisa AsaiDepartment of Respiratory Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka-City, Osaka, 545-8585, Japan.
Kazuto HirataDepartment of Respiratory Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka-City, Osaka, 545-8585, Japan.
Kenji KangawaDepartment of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, 5-7-1, Fujishirodai, Suita-City, Osaka, 565-8565, Japan.
National Cerebral and Cardiovascular Center · JPOsaka City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPulmonary fibrosis is a life-threatening disease characterized by progressive dyspnea and worsening pulmonary function. Atrial natriuretic peptide (ANP), a heart-derived secretory peptide used clinically in Japan for the treatment of acute heart failure, exerts a wide range of protective effects on various organs, including the heart, blood vessels, kidneys, and lungs. Its therapeutic properties are characterized by anti-inflammatory and anti-fibrotic activities mediated by the guanylyl cyclase-A (GC-A) receptor. We hypothesized that ANP would have anti-fibrotic and anti-inflammatory effects on bleomycin (BLM)-induced pulmonary fibrosis in mice.

methodsMice were divided into three groups: normal control, BLM with vehicle, and BLM with ANP. ANP (0.5 μg/kg/min via osmotic-pump, subcutaneously) or vehicle administration was started before BLM administration (1 mg/kg) and continued until the mice were sacrificed. At 7 or 21 days after BLM administration, fibrotic changes and infiltration of inflammatory cells in the lungs were assessed based on histological findings and analysis of bronchoalveolar lavage fluid. In addition, fibrosis and inflammation induced by BLM were evaluated in vascular endothelium-specific GC-A overexpressed mice. Finally, attenuation of transforming growth factor-β (TGF-β) signaling by ANP was studied using immortalized mouse endothelial cells stably expressing GC-A receptor.

resultsANP significantly decreased lung fibrotic area and infiltration of inflammatory cells in lungs after BLM administration. Furthermore, similar effects of ANP were observed in vascular endothelium-specific GC-A overexpressed mice. In cultured mouse endothelial cells, ANP reduced phosphorylation of Smad2 after TGF-β stimulation.

conclusionsANP exerts protective effects on BLM-induced pulmonary fibrosis via vascular endothelial cells.

Indexed as

AnimalsAtrial Natriuretic FactorBleomycinEndothelial CellsImmunologic FactorsLungMaleMiceMice, Inbred C57BLPulmonary FibrosisTreatment OutcomeAtrial Natriuretic FactorBleomycinImmunologic FactorsAtrial natriuretic peptideBleomycinPulmonary fibrosisTransforming growth factor-βVascular endothelial cell

Identifiers

PMID28049526
PMCPMC5210263
OpenAlexW2565119551

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LicenceCC BY
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Registered trials

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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.