The Role of Lipotoxicity in Smoke Cardiomyopathy

Detalhes bibliográficos
Autor(a) principal: Santos, Priscila P. [UNESP]
Data de Publicação: 2014
Outros Autores: Oliveira, Fernando [UNESP], Ferreira, Vanessa C. M. P. [UNESP], Polegato, Bertha Furlan [UNESP], Roscani, Meliza Goi [UNESP], Fernandes, Ana Angelica [UNESP], Modesto, Pamela [UNESP], Rafacho, Bruna P. M. [UNESP], Zanati, Silmeia G. [UNESP], Di Lorenzo, Annarita, Matsubara, Luiz Shiguero [UNESP], Paiva, Sergio Alberto Rupp de [UNESP], Zornoff, Leonardo Antonio Mamede [UNESP], Minicucci, Marcos Ferreira [UNESP], Gaiolla, Paula Schmidt Azevedo [UNESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.1371/journal.pone.0113739
http://hdl.handle.net/11449/117417
Resumo: Background/Aims: Experimental 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.Methods: Wistar rats were allocated to control (C) and cigarette smoke (CS) groups. CS rats were exposed to cigarette smoke for 2 months.Results: After 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 (PPAR alpha) and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1 alpha) 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.Conclusion: The 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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spelling The Role of Lipotoxicity in Smoke CardiomyopathyBackground/Aims: Experimental 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.Methods: Wistar rats were allocated to control (C) and cigarette smoke (CS) groups. CS rats were exposed to cigarette smoke for 2 months.Results: After 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 (PPAR alpha) and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1 alpha) 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.Conclusion: The cardiac remodeling that was observed in the CS exposure model may be explained by abnormalities in energy metabolism, including lipotoxicity and oxidative stress.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Botucatu Medical School, UNESP - Univ Estadual Paulista, Botucatu, Sao Paulo, BrasilUNESP Univ Estadual Paulista, Botucatu Med Sch, Dept Internal Med, Botucatu, SP, BrazilUNESP Univ Estadual Paulista, Inst Biociencias Botucatu, Dept Chem & Biochem, Botucatu, SP, BrazilCornell Univ, Weill Med Coll, Ctr Vasc Biol, Dept Pathol & Lab Med, New York, NY 10021 USAUNESP Univ Estadual Paulista, Botucatu Med Sch, Dept Internal Med, Botucatu, SP, BrazilUNESP Univ Estadual Paulista, Inst Biociencias Botucatu, Dept Chem & Biochem, Botucatu, SP, BrazilPublic Library ScienceUniversidade Estadual Paulista (Unesp)Cornell UnivSantos, Priscila P. [UNESP]Oliveira, Fernando [UNESP]Ferreira, Vanessa C. M. P. [UNESP]Polegato, Bertha Furlan [UNESP]Roscani, Meliza Goi [UNESP]Fernandes, Ana Angelica [UNESP]Modesto, Pamela [UNESP]Rafacho, Bruna P. M. [UNESP]Zanati, Silmeia G. [UNESP]Di Lorenzo, AnnaritaMatsubara, Luiz Shiguero [UNESP]Paiva, Sergio Alberto Rupp de [UNESP]Zornoff, Leonardo Antonio Mamede [UNESP]Minicucci, Marcos Ferreira [UNESP]Gaiolla, Paula Schmidt Azevedo [UNESP]2015-03-18T15:56:05Z2015-03-18T15:56:05Z2014-12-02info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article13application/pdfhttp://dx.doi.org/10.1371/journal.pone.0113739Plos One. San Francisco: Public Library Science, v. 9, n. 12, 13 p., 2014.1932-6203http://hdl.handle.net/11449/11741710.1371/journal.pone.0113739WOS:000345869700045WOS000345869700045.pdf63098351379987665016839015394547121314080140264774387040344716730000-0002-5843-6232Web of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengPlos One2.7661,164info:eu-repo/semantics/openAccess2024-08-14T17:22:25Zoai:repositorio.unesp.br:11449/117417Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-14T17:22:25Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv The Role of Lipotoxicity in Smoke Cardiomyopathy
title The Role of Lipotoxicity in Smoke Cardiomyopathy
spellingShingle The Role of Lipotoxicity in Smoke Cardiomyopathy
Santos, Priscila P. [UNESP]
title_short The Role of Lipotoxicity in Smoke Cardiomyopathy
title_full The Role of Lipotoxicity in Smoke Cardiomyopathy
title_fullStr The Role of Lipotoxicity in Smoke Cardiomyopathy
title_full_unstemmed The Role of Lipotoxicity in Smoke Cardiomyopathy
title_sort The Role of Lipotoxicity in Smoke Cardiomyopathy
author Santos, Priscila P. [UNESP]
author_facet Santos, Priscila P. [UNESP]
Oliveira, Fernando [UNESP]
Ferreira, Vanessa C. M. P. [UNESP]
Polegato, Bertha Furlan [UNESP]
Roscani, Meliza Goi [UNESP]
Fernandes, Ana Angelica [UNESP]
Modesto, Pamela [UNESP]
Rafacho, Bruna P. M. [UNESP]
Zanati, Silmeia G. [UNESP]
Di Lorenzo, Annarita
Matsubara, Luiz Shiguero [UNESP]
Paiva, Sergio Alberto Rupp de [UNESP]
Zornoff, Leonardo Antonio Mamede [UNESP]
Minicucci, Marcos Ferreira [UNESP]
Gaiolla, Paula Schmidt Azevedo [UNESP]
author_role author
author2 Oliveira, Fernando [UNESP]
Ferreira, Vanessa C. M. P. [UNESP]
Polegato, Bertha Furlan [UNESP]
Roscani, Meliza Goi [UNESP]
Fernandes, Ana Angelica [UNESP]
Modesto, Pamela [UNESP]
Rafacho, Bruna P. M. [UNESP]
Zanati, Silmeia G. [UNESP]
Di Lorenzo, Annarita
Matsubara, Luiz Shiguero [UNESP]
Paiva, Sergio Alberto Rupp de [UNESP]
Zornoff, Leonardo Antonio Mamede [UNESP]
Minicucci, Marcos Ferreira [UNESP]
Gaiolla, Paula Schmidt Azevedo [UNESP]
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade Estadual Paulista (Unesp)
Cornell Univ
dc.contributor.author.fl_str_mv Santos, Priscila P. [UNESP]
Oliveira, Fernando [UNESP]
Ferreira, Vanessa C. M. P. [UNESP]
Polegato, Bertha Furlan [UNESP]
Roscani, Meliza Goi [UNESP]
Fernandes, Ana Angelica [UNESP]
Modesto, Pamela [UNESP]
Rafacho, Bruna P. M. [UNESP]
Zanati, Silmeia G. [UNESP]
Di Lorenzo, Annarita
Matsubara, Luiz Shiguero [UNESP]
Paiva, Sergio Alberto Rupp de [UNESP]
Zornoff, Leonardo Antonio Mamede [UNESP]
Minicucci, Marcos Ferreira [UNESP]
Gaiolla, Paula Schmidt Azevedo [UNESP]
description Background/Aims: Experimental 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.Methods: Wistar rats were allocated to control (C) and cigarette smoke (CS) groups. CS rats were exposed to cigarette smoke for 2 months.Results: After 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 (PPAR alpha) and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1 alpha) 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.Conclusion: The cardiac remodeling that was observed in the CS exposure model may be explained by abnormalities in energy metabolism, including lipotoxicity and oxidative stress.
publishDate 2014
dc.date.none.fl_str_mv 2014-12-02
2015-03-18T15:56:05Z
2015-03-18T15:56:05Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.1371/journal.pone.0113739
Plos One. San Francisco: Public Library Science, v. 9, n. 12, 13 p., 2014.
1932-6203
http://hdl.handle.net/11449/117417
10.1371/journal.pone.0113739
WOS:000345869700045
WOS000345869700045.pdf
6309835137998766
5016839015394547
1213140801402647
7438704034471673
0000-0002-5843-6232
url http://dx.doi.org/10.1371/journal.pone.0113739
http://hdl.handle.net/11449/117417
identifier_str_mv Plos One. San Francisco: Public Library Science, v. 9, n. 12, 13 p., 2014.
1932-6203
10.1371/journal.pone.0113739
WOS:000345869700045
WOS000345869700045.pdf
6309835137998766
5016839015394547
1213140801402647
7438704034471673
0000-0002-5843-6232
dc.language.iso.fl_str_mv eng
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dc.publisher.none.fl_str_mv Public Library Science
publisher.none.fl_str_mv Public Library Science
dc.source.none.fl_str_mv Web of Science
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