Evidence map›Paper›PMID 23431404›Full record

ArticlePloS one2013

Cardiac-specific overexpression of metallothionein rescues against cigarette smoking exposure-induced myocardial contractile and mitochondrial damage.

Nan Hu, Xuefeng Han, Erin K Lane, Feng Gao, Yingmei Zhang, Jun Ren

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Cigarette exposure lights the NLPR3 inflammasome pathway to atrial fibrillation.American journal of physiology. Heart and circulatory physiology · 2025
    Article
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  20. Recent advances in pre-clinical mouse models of COPD.Clinical science (London, England : 1979) · 2014
    Review
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

6 authors at 2 institutions in 2 countries.

Nan HuCenter for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, Wyoming, United States of America.
Xuefeng Han
Erin K Lane
Feng Gao
Yingmei Zhang
Jun Ren
University of Wyoming · USAir Force Medical University · CN

Funding

Wyoming IDeA Networks of Biomedical Research ExcellenceP20RR016474 · NCRR · UNIVERSITY OF WYOMING · PI REN, JUN · 2001 to 2011
$28.2M
NCRR NIH HHS NIH 5P20RR016474NCRR NIH HHS P20 RR016474
6 · The paper itself

Abstract

objectivesSecond hand cigarette smoke is an independent risk factor for cardiovascular disease. Although a tie between smoking and cardiovascular disease is well established, the underlying mechanisms still remains elusive due to the lack of adequate animal models. This study was designed to use a mouse model of exposure to cigarette smoke, a surrogate of environmental tobacco smoke, to evaluate the impact of cardiac overexpression of heavy metal scavenger metallothionein on myocardial geometry, contractile and intracellular Ca(2+) properties and apoptosis following side-stream smoke exposure.

methodsAdult male wild-type FVB and metallothionein transgenic mice were placed in a chamber exposed to cigarette smoke for 1 hour daily for 40 days. Echocardiographic, cardiomyocyte contractile and intracellular Ca(2+) properties, fibrosis, apoptosis and mitochondrial damage were examined.

resultsOur data revealed that smoke exposure enlarged ventricular end systolic and diastolic diameters, reduced myocardial and cardiomyocyte contractile function, disrupted intracellular Ca(2+) homeostasis, facilitated fibrosis, apoptosis and mitochondrial damage (cytochrome C release and aconitase activity), the effects of which were attenuated or mitigated by metallothionein. In addition, side-stream smoke expose enhanced phosphorylation of Akt and GSK3β without affecting pan protein expression in the heart, the effect of which was abolished or ameliorated by metallothionein. Cigarette smoke extract interrupted cardiomyocyte contractile function and intracellular Ca(2+) properties, the effect of which was mitigated by wortmannin and NAC.

conclusionsThese data suggest that side-stream smoke exposure led to myocardial dysfunction, intracellular Ca(2+) mishandling, apoptosis, fibrosis and mitochondrial damage, indicating the therapeutic potential of antioxidant against in second smoking-induced cardiac defects possibly via mitochondrial damage and apoptosis.

Indexed as

Myocardial ContractionAconitate HydrataseAnimalsAntioxidantsApoptosisApoptosis Regulatory ProteinsCalciumCalcium-Binding ProteinsCalcium SignalingCardiovascular DiseasesCells, CulturedCytochromes cFibrosisMaleMetallothioneinMiceAconitate HydrataseAntioxidantsApoptosis Regulatory ProteinsCalciumCalcium-Binding ProteinsCytochromes cMetallothioneinNitric Oxide Synthase Type IIINos3 protein, mousePhospholambanReactive Oxygen SpeciesSarcoplasmic Reticulum Calcium-Transporting ATPasesTobacco Smoke Pollution

Identifiers

PMID23431404
PMCPMC3576371
OpenAlexW2016769652

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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.