ArticlePloS one2014
The role of lipotoxicity in smoke cardiomyopathy.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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Who cites it
19 citing papers in PubMed, 48 citations in OpenAlex.
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- Widespread chromosomal rearrangements preceded genetic divergence in a monitor lizard, Varanus acanthurus (Varanidae).Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Article
- Sodium-Glucose Cotransporter 2 Inhibitors and Cardiac Remodeling.Journal of cardiovascular translational research · 2022Review
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- Sex differences in cardiac remodeling post myocardial infarction with acute cigarette smoking.Biology of sex differences · 2022Article
- Electronic and Tobacco Cigarettes Alter Polyunsaturated Fatty Acids and Oxidative Biomarkers.Circulation research · 2021Article
- Vitamin D Supplementation Induces Cardiac Remodeling in Rats: Association with Thioredoxin-Interacting Protein and Thioredoxin.Arquivos brasileiros de cardiologia · 2021Article
- The role of glucose metabolism and insulin resistance in cardiac remodelling induced by cigarette smoke exposure.Journal of cellular and molecular medicine · 2021Article
- Cocoa Flavonoids Reduce Inflammation and Oxidative Stress in a Myocardial Ischemia-Reperfusion Experimental Model.Antioxidants (Basel, Switzerland) · 2020Article
- The flavoring and not the nicotine content is a decisive factor for the effects of refill liquids of electronic cigarette on the redox status of endothelial cells.Toxicology reports · 2020Article
- Short-Term Cigarette Smoking in Rats Impairs Physical Capacity and Induces Cardiac Remodeling.BioMed research international · 2020Article
- Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke.BMC pharmacology & toxicology · 2018Article
- Spondias mombin supplementation attenuated cardiac remodelling process induced by tobacco smoke.Journal of cellular and molecular medicine · 2018Article
- Editorial: Cardiac Remodeling: New Insights in Physiological and Pathological Adaptations.Frontiers in physiology · 2017Article
- Functional, Cellular, and Molecular Remodeling of the Heart under Influence of Oxidative Cigarette Tobacco Smoke.Oxidative medicine and cellular longevity · 2017Review
- Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure.Arquivos brasileiros de cardiologia · 2016Article
- Cardiac Remodeling: Concepts, Clinical Impact, Pathophysiological Mechanisms and Pharmacologic Treatment.Arquivos brasileiros de cardiologia · 2016Review
- Article
- Change in left ventricular systolic function in patients with ST elevation myocardial infarction: Evidence for smoker's paradox or pseudo-paradox?Indian heart journalArticle
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsExperimental and clinical studies have shown the direct toxic effects of cigarette smoke (CS) on the myocardium, independent of vascular effects. However, the underlying mechanisms are not well known.
methodsWistar rats were allocated to control (C) and cigarette smoke (CS) groups. CS rats were exposed to cigarette smoke for 2 months.
resultsAfter that morphometric, functional and biochemical parameters were measured. The echocardiographic study showed enlargement of the left atria, increase in the left ventricular systolic volume and reduced systolic function. Within the cardiac metabolism, exposure to CS decreased beta hydroxy acyl coenzyme A dehydrogenases and citrate synthases and increased lactate dehydrogenases. Peroxisome proliferator-activated receptor alpha (PPARα) and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) were expressed similarly in both groups. CS increased serum lipids and myocardial triacylglycerols (TGs). These data suggest that impairment in fatty acid oxidation and the accumulation of cardiac lipids characterize lipotoxicity. CS group exhibited increased oxidative stress and decreased antioxidant defense. Finally, the myocyte cross-sectional area and active Caspase 3 were increased in the CS group.
conclusionThe cardiac remodeling that was observed in the CS exposure model may be explained by abnormalities in energy metabolism, including lipotoxicity and oxidative stress.
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Registered trials
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