Evidence map›Paper›PMID 26899624›Full record

ArticleLung2016

Impaired Lung Mitochondrial Respiration Following Perinatal Nicotine Exposure in Rats.

Daniel T Cannon, Jie Liu, Reiko Sakurai, Harry B Rossiter, Virender K Rehan

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Lung, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. 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

5 authors at 2 institutions in 2 countries.

Daniel T CannonDivision of Respiratory & Critical Care Physiology & Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA, 90502, USA. dcannon@mail.sdsu.edu.ORCID http://orcid.org/0000-0002-2175-3445
Jie LiuDivision of Neonatology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA, 90502, USA.
Reiko SakuraiDivision of Neonatology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA, 90502, USA.
Harry B RossiterDivision of Respiratory & Critical Care Physiology & Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA, 90502, USA.
Virender K RehanDivision of Neonatology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA, 90502, USA.
The Lundquist Institute · USUniversity of Leeds · GB

Funding

Developmental Nicotine Exposure & Transgenerationally Altered Lung PhenotypeR01HL127237 · NHLBI · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI REHAN, VIRENDER K · 2016 to 2019
$1.8M
Fibroblast Cell Signaling in Utero Nicotine-Induced Lung InjuryR01HD051857 · NICHD · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI REHAN, VIRENDER K · 2008 to 2012
$1.7M
In Utero Nicotine Exposure & Transgenerational Transmission of AsthmaR21HD071731 · NICHD · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI REHAN, VIRENDER K · 2012 to 2013
$369k
NHLBI NIH HHS R01 HL127237NICHD NIH HHS HD51857NICHD NIH HHS HD71731NICHD NIH HHS R01 HD051857NICHD NIH HHS R21 HD071731
6 · The paper itself

Abstract

Perinatal smoke/nicotine exposure predisposes to chronic lung disease and morbidity. Mitochondrial abnormalities may contribute as the PPARγ pathway is involved in structural and functional airway deficits after perinatal nicotine exposure. We hypothesized perinatal nicotine exposure results in lung mitochondrial dysfunction that can be rescued by rosiglitazone (RGZ; PPARγ receptor agonist). Sprague-Dawley dams received placebo (CON), nicotine (NIC, 1 mg kg(-1)), or NIC + RGZ (3 mg kg(-1)) daily from embryonic day 6 to postnatal day 21. Parenchymal lung (~10 mg) was taken from adult male offspring for mitochondrial assessment in situ. ADP-stimulated O2 consumption was less in NIC and NIC + RGZ compared to CON (F[2,14] = 17.8; 4.5 ± 0.8 and 4.1 ± 1.4 vs. 8.8 ± 2.5 pmol s mg(-1); p < 0.05). The respiratory control ratio for ADP, an index of mitochondrial coupling, was reduced in NIC and remediated in NIC + RGZ (F[2,14] = 3.8; p < 0.05). Reduced mitochondrial oxidative capacity and abnormal coupling were evident after perinatal nicotine exposure. RGZ improved mitochondrial function through tighter coupling of oxidative phosphorylation.

Indexed as

Prenatal Exposure Delayed EffectsAnimalsAnimals, NewbornCell RespirationFemaleGestational AgeLungMaternal ExposureMitochondriaNicotineNicotinic AgonistsOxidative PhosphorylationPPAR gammaPregnancyRats, Sprague-DawleyRosiglitazoneNicotineNicotinic AgonistsPPAR gammaRosiglitazoneThiazolidinediones

Identifiers

PMID26899624
PMCPMC4799736
OpenAlexW2285185374

What OpenQuestion holds

Textmetadata
LicenceTDM
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.