Evidence map›Paper›PMID 21057039›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2011

Chronic cigarette smoking causes hypertension, increased oxidative stress, impaired NO bioavailability, endothelial dysfunction, and cardiac remodeling in mice.

M A Hassan Talukder, Wesley M Johnson, Saradhadevi Varadharaj, Jiarui Lian, Patrick N Kearns, Mohamed A El-Mahdy, Xiaoping Liu, Jay L Zweier

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed
9.7field-weighted citation impact, top 1% 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

130 citing papers in PubMed, 288 citations in OpenAlex.

  1. Cigarette Smoking Blunts Exercise-Induced Heart Rate Response among Young Adult Male Smokers.International journal of environmental research and public health · 2019
    Trial
  2. Trial
  3. Article
  4. Review
  5. Laboratory Analysis of FecalHealth science reports · 2026
    Article
  6. Smoking Cessation, Weight Change, and Risk of Dementia: A Prospective Cohort Study.medRxiv : the preprint server for health sciences · 2025
    Article
  7. Article
  8. Review
  9. Investigation of 5-fluorouracil cardiotoxicity in combinational therapy: Influence of risk factors and demographics in a Pakistani population.Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners · 2025
    Article
  10. Review
  11. Article
  12. Mitigation of nicotine-induced podocyte injury through inhibition of thioredoxin interacting protein.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
    Article
  13. Review
  14. Article
  15. Tobacco cigarette smoking induces cerebrovascular dysfunction followed by oxidative neuronal injury with the onset of cognitive impairment.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025
    Article
  16. Article
  17. Review
  18. Cardiac diastolic dysfunction by cigarette smoking is associated with mitochondrial integrity in the heart.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  19. Article
  20. Construction of a Nomogram-Based Prediction Model for the Risk of Diabetic Kidney Disease in T2DM.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Article

70 more citing papers are in PubMed but not listed here.

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

8 authors at 1 institution in 1 country.

M A Hassan TalukderCenter for Environmental and Smoking-Induced Diseases, Davis Heart and Lung Research Institute, and Division of Cardiovascular Medicine, Department of Internal Medicine, The Ohio State University College of Medicine, Columbus, Ohio 43210, USA.
Wesley M Johnson
Saradhadevi Varadharaj
Jiarui Lian
Patrick N Kearns
Mohamed A El-Mahdy
Xiaoping Liu
Jay L Zweier
The Ohio State University · US

Funding

Stat3 in Post-Ischemic Myocardial InflammationP01HL065608 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BECKER, LEWIS C · 2000 to 2011
$22.0M
OXYGEN RADICALS AND NITRIC OXIDE IN POSTISCHEMIC INJURYR01HL063744 · NHLBI · OHIO STATE UNIVERSITY · PI ZWEIER, JAY LOUIS · 2000 to 2009
$5.2M
MEASURE OF FREE RADICAL GENERATION IN HEARTR01HL038324 · NHLBI · OHIO STATE UNIVERSITY · PI ZWEIER, JAY LOUIS · 1992 to 2010
$3.5M
Proton Electron Double Resonance Imaging (PEDRI) of Free RadicalsR01EB004900 · NIBIB · OHIO STATE UNIVERSITY · PI ZWEIER, JAY LOUIS · 2005 to 2008
$3.4M
In Vivo EPR/NMR Co-Imaging of Free RadicalsR01EB000890 · NIBIB · OHIO STATE UNIVERSITY · PI ZWEIER, JAY LOUIS · 2002 to 2005
$2.9M
MEASUREMENT OF FREE RADICAL GENERATION IN THE HEARTR29HL038324 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI ZWEIER, JAY LOUIS · 1987 to 1991
–
NHLBI NIH HHS HL-38324NHLBI NIH HHS HL-63744NHLBI NIH HHS HL-65608NIBIB NIH HHS EB-0890NIBIB NIH HHS EB-4900
6 · The paper itself

Abstract

Cigarette smoking is a major independent risk factor for cardiovascular disease. While the association between chronic smoking and cardiovascular disease is well established, the underlying mechanisms are incompletely understood, partly due to the lack of adequate in vivo animal models. Here, we report a mouse model of chronic smoking-induced cardiovascular pathology. Male C57BL/6J mice were exposed to whole body mainstream cigarette smoke (CS) using a SCIREQ "InExpose" smoking system (48 min/day, 5 days/wk) for 16 or 32 wk. Age-matched, air-exposed mice served as nonsmoking controls. Blood pressure was measured, and cardiac MRI was performed. In vitro vascular ring and isolated heart experiments were performed to measure vascular reactivity and cardiac function. Blood from control and smoking mice was studied for the nitric oxide (NO) decay rate and reactive oxygen species (ROS) generation. With 32 wk of CS exposure, mice had significantly less body weight gain and markedly higher blood pressure. At 32 wk of CS exposure, ACh-induced vasorelaxation was significantly shifted to the right and downward, left ventricular mass was significantly larger along with an increased heart-to-body weight ratio, in vitro cardiac function tended to be impaired with high afterload, white blood cells had significantly higher ROS generation, and the blood NO decay rate was significantly faster. Thus, smoking led to blunted weight gain, hypertension, endothelial dysfunction, leukocyte activation with ROS generation, decreased NO bioavailability, and mild cardiac hypertrophy in mice that were not otherwise predisposed to disease. This mouse model is a useful tool to enable further elucidation of the molecular and cellular mechanisms of smoking-induced cardiovascular diseases.

Indexed as

Oxidative StressVentricular RemodelingAnalysis of VarianceAnimalsBlood PressureBody WeightEndothelium, VascularHeartHypertensionMagnetic Resonance ImagingMaleMiceMyocardiumNicotianaNitric OxideReactive Oxygen SpeciesNitric OxideReactive Oxygen SpeciesSmoke

Identifiers

PMID21057039
PMCPMC3023256
OpenAlexW2104716397

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.