Evidence map›Paper›PMID 17089097›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2006

Effects of olmesartan, an AT1 receptor antagonist, on hypoxia-induced activation of ERK1/2 and pro-inflammatory signals in the mouse lung.

Yoshiyuki Tanabe, Yuki Morikawa, Takao Kato, Satoshi Kanai, Taichi Watakabe, Ami Nishijima, Hijiri Iwata, Kaori Isobe, Mayumi Ishizaki, Koichi Nakayama

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Neurohormonal modulation in pulmonary arterial hypertension.The European respiratory journal · 2021
    Review
  5. Candesartan could ameliorate the COVID-19 cytokine storm.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2020
    Article
  6. Article
  7. Article
  8. Angiotensin II type 1 receptor blockade partially attenuates hypoxia-induced pulmonary hypertension in newborn piglets: relationship with the nitrergic system.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2012
    Article
  9. Article
  10. Protective effects of L-type fatty acid-binding protein (L-FABP) in proximal tubular cells against glomerular injury in anti-GBM antibody-mediated glomerulonephritis.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2011
    Article
  11. 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

10 authors at 1 institution in 1 country.

Yoshiyuki TanabeDepartment of Cellular and Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku, Shizuoka-shi, Shizuoka, 422-8526, Japan.
Yuki Morikawa
Takao Kato
Satoshi Kanai
Taichi Watakabe
Ami Nishijima
Hijiri Iwata
Kaori Isobe
Mayumi Ishizaki
Koichi Nakayama
University of Shizuoka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to investigate the effects of olmesartan, an antagonist for angiotensin II receptor type 1(AT1), on the activation of extracellular signal-regulated kinases (ERK)1/2, tissue remodeling, and pro-inflammatory signals in the right ventricle and lung of mice during the early phase of hypobaric hypoxia. Phosphorylation of ERK1/2 in both tissue types in response to hypoxia peaked at 1-3 days, and declined rapidly in the right ventricle, whereas in the lung it was sustained for at least 8 days. Upregulation of angiotensinogen mRNA was observed in the hypoxic lung at 4-9 days, but not in the hypoxic right ventricle and pulmonary artery. Olmesartan inhibited the hypoxia-induced phosphorylation of ERK1/2 in the lung, but not in the right ventricle. Neither right ventricular hypertrophy nor the thickening of the intrapulmonary arterial wall was ameliorated by olmesartan. However, this drug inhibited the expression of the mRNA for angiotensinogen and several pro-inflammatory factors, including interleukin-6 and inducible nitric oxide synthase in the hypoxic lung. These results suggest that olmesartan blocks a potential positive feedback loop of the angiotensin II-AT1 receptor system, which may lead to attenuate pro-inflammatory signals in the mouse lung, that are associated with hypoxic pulmonary hypertension, without inducing any appreciable effects on the compensatory cardiopulmonary hypertrophy at an early phase of exposure to a hypobaric hypoxic environment.

Indexed as

Angiotensin II Type 1 Receptor BlockersAngiotensinogenAnimalsGene Expression RegulationHeart VentriclesHypertension, PulmonaryHypoxiaImidazolesInflammation MediatorsLungMaleMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Olmesartan MedoxomilPhosphorylationAngiotensin II Type 1 Receptor BlockersAngiotensinogenImidazolesInflammation MediatorsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Olmesartan MedoxomilRNA, MessengerTetrazoles

Identifiers

PMID17089097
OpenAlexW2024401820

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.