Evidence map›Paper›PMID 25647402›Full record

ArticleAmerican journal of respiratory cell and molecular biology2015

Enhanced Resolution of Hyperoxic Acute Lung Injury as a result of Aspirin Triggered Resolvin D1 Treatment.

Ruan Cox, Oluwakemi Phillips, Jutaro Fukumoto, Itsuko Fukumoto, Prasanna Tamarapu Parthasarathy, Stephen Arias, Young Cho, Richard F Lockey, Narasaiah Kolliputi

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
7.7field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 78 citations in OpenAlex.

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  14. Lung fibrosis is induced in ADAR2 overexpressing mice via HuR-induced CTGF signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
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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

9 authors at 1 institution in 1 country.

Ruan CoxDepartments of 1 Internal Medicine and.
Oluwakemi PhillipsDepartments of 1 Internal Medicine and.
Jutaro FukumotoDepartments of 1 Internal Medicine and.
Itsuko FukumotoDepartments of 1 Internal Medicine and.
Prasanna Tamarapu ParthasarathyDepartments of 1 Internal Medicine and.
Stephen AriasDepartments of 1 Internal Medicine and.
Young ChoDepartments of 1 Internal Medicine and.
Richard F LockeyDepartments of 1 Internal Medicine and.
Narasaiah KolliputiDepartments of 1 Internal Medicine and.
University of South Florida · US

Funding

Molecular Mechanisms of Hyperoxic Lung InjuryR01HL105932 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI KOLLIPUTI, NARASAIAH · 2011 to 2019
$2.9M
NHLBI NIH HHS R01 HL105932
6 · The paper itself

Abstract

Acute lung injury (ALI), which presents as acute respiratory failure, is a major clinical problem that requires aggressive care, and patients who require prolonged oxygen exposure are at risk of developing this disease. Although molecular determinants of ALI have been reported, the molecules involved in disease catabasis associated with oxygen toxicity have not been well studied. It has been reported that lung mucosa is rich in omega-3 fatty acid dicosahexanoic acid (DHA), which has antiinflammatory properties. Aspirin-triggered resolvin D1 (AT-RvD1) is a potent proresolution metabolite of DHA that can curb the inflammatory effects in various acute injuries, yet the effect of AT-RvD1 on hyperoxic acute lung injury (HALI) or in the oxygen toxicity setting in general has not been investigated. The effects of AT-RvD1 on HALI were determined for the first time in 8- to 10-week-old C57BL/6 mice that were exposed to hyperoxia (≥95% O2) for 48 hours. Mice were given AT-RvD1 (100 ng) in saline or a saline vehicle for 24 hours in normoxic (≈21% O2) conditions after hyperoxia. Lung tissue and bronchoalveolar lavage (BAL) fluid were collected for analysis associated with proinflammatory signaling and lung inflammation. AT-RvD1 treatment resulted in reduced oxidative stress, increased glutathione production, and significantly decreased tissue inflammation. AT-RvD1 treatment also significantly reduced the lung wet/dry ratio, protein in BAL fluid, and decreased apoptotic and NF-κB signaling. These results show that AT-RvD1 curbs oxygen-induced lung edema, permeability, inflammation, and apoptosis and is thus an effective therapy for prolonged hyperoxia exposure in this murine model.

Indexed as

Acute Lung InjuryAirway ResistanceAnimalsAnti-Inflammatory Agents, Non-SteroidalApoptosisAspirinDocosahexaenoic AcidsDrug Evaluation, PreclinicalHyperoxiaLungMice, Inbred C57BLNeutrophil InfiltrationOxidative StressAnti-Inflammatory Agents, Non-SteroidalAspirinDocosahexaenoic Acidsresolvin D1acute lung injuryhyperoxiaresolvin

Identifiers

PMID25647402
PMCPMC4566067
OpenAlexW1927386097

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.