The Role of Lipotoxicity in Smoke Cardiomyopathy

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.

Spondias mombin supplementation attenuated cardiac remodelling process induced by tobacco smoke

“…Experimental studies showed that lipotoxicity, oxidative stress, inflammation, hemodynamic overload and increased expression of mitogen‐activated protein kinases (MAPK) are important mechanistic pathways linked with the effects of tobacco smoke on cardiac remodelling . To attenuate this process, the supplementation of antioxidant and anti‐inflammatory substances, such as vitamin D, beta‐carotene, retinoic acid and taurine, has been studied .…”

Cardiac Remodeling Induced by All-Trans Retinoic Acid is Detrimental in Normal Rats

“…Glutathione peroxidase (GSHPx, E.C.1.11.1.9), superoxide dismutase (SOD, E.C.1.15.1.1), and catalase (CAT, E.C.1.11.1.6) activity was assessed as previously specified [26]. The cardiac energy metabolism was assessed with 3-hydroxyacyl coenzyme-A dehydrogenase (OHADH, E.C.1.1.1.35.)…”

Green tea (Cammellia sinensis) attenuates ventricular remodeling after experimental myocardial infarction

“…Collagen fractional area was analyzed in tissues stained with Picro Sirius red as described previously, in remote areas free from MI [21]. Immunofluorescence staining was used to evaluate myocyte cross sectional area (CSA) and capillary-to-myocytes ratio, as described previously [7,22,23]. Images were acquired using Olympus Fluorescence microscope BX51 (Olympus Latin America Inc.).…”

“…Wheat germ agglutinin fluorescein isothiocyanate (FITC) labeled (WGA-FITC -Sigma-Aldrich Co. LLC. L4895) was used to stain cardiac myocytes [7]. Image-Pro Plus 3.0 (Media Cybernetics, Silver Spring, MD) was used to measure myocyte area.…”

“…This change protects the heart, in part, because FAs waste more oxygen to be oxidized. However, over time, while not oxidized, FAs accumulate inside myocytes, leading to cardiac lipotoxicity [6,7]. Lipotoxicity is a potential inductor of apoptosis and dysfunction.…”