The Role of Lipotoxicity in Smoke Cardiomyopathy

PLoS One

Ana Angelica Fernandes¹  Annarita Di Lorenzo²  Meliza G. Roscani³  Paula S. Azevedo³  Bruna P. M. Rafacho³  Vanessa C. M. P. Ferreira³  Silmeia G. Zanati³  Luiz S. Matsubara³  Leonardo A. M. Zornoff³  Pamela Modesto³  Sergio A. R. Paiva³  Priscila P. Santos³  Bertha F. Polegato³  Marcos F. Minicucci³  Fernando Oliveira³ 

[1] Chemistry and Biochemistry Department, Instituto de Biociências de Botucatu, UNESP - Universidade Estadual Paulista, Botucatu, São Paulo, Brazil;Department of Pathology and Laboratory Medicine, Center of Vascular Biology, Weill Medical College of Cornell University, New York, New York, United States of America;Internal Medicine Department, Botucatu Medical School, UNESP - Universidade Estadual Paulista, Botucatu, São Paulo, Brazil

关键词: Smoking habits;    Apoptosis;    Mitochondria;    Oxidative stress;    Muscle cells;    Energy metabolism;    Oxidation;    Lipids;   

DOI  :  10.1371/journal.pone.0113739

学科分类：医学（综合）

来源: Public Library of Science

【 摘 要 】

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 (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.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.

【 授权许可】

CC BY