Analysis of probable lipotoxic damage and myocardial fibrosis in epicardial obesity.
Analysis of probable lipotoxic damage and myocardial fibrosis in epicardial obesity.
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DOI：
10.18632/aging.203148
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发表时间：
2021-06-04
期刊：
影响因子：
--
通讯作者：
Dyleva Y
中科院分区：
文献类型：
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作者：
Chumakova G;Gritsenko O;Gruzdeva O;Dyleva Y
心肌纤维化被认为是心血管疾病发展的关键病理过程。在心外膜肥胖（EO）中，纤维化发展的主要原因是脂毒性心肌损伤。使用无创诊断方法在早期检测心肌纤维化是很重要的。根据超声心动图（ECG）结果，将110例一般性肥胖男性分为心外膜脂肪厚度(tEAT)≥7 mm组（n = 70）和无舒张功能障碍的tEAT < 7 mm组（n = 40）。测定两组的代谢因子、促炎细胞因子、脂肪因子、游离脂肪酸（FFA）、促纤维化标志物的水平。I组与II组比较，白细胞介素(IL)-6、c反应蛋白、肿瘤坏死因子(TNF)-α水平升高，瘦素、脂联素水平降低。ⅰ组各促纤维化因子水平均升高，TNF-α、IL-6水平与瘦素、FFA水平呈正相关，与脂联素水平呈负相关。我们还观察到胶原蛋白、转化生长因子(TGF)-β和金属蛋白酶(MMP)-3水平与EO之间的关系。我们的研究结果表明，证实的EO不仅与脂肪分解和促炎细胞因子水平升高有关，而且与促纤维化因子水平升高有关。这表明所研究的纤维化标志物可用于确定EO患者伴脂毒性心肌损伤的临床前心脏纤维化。
Myocardial fibrosis is considered a key pathological process in the development of cardiovascular diseases. In epicardial obesity (EO), the main cause of fibrosis development is lipotoxic myocardial damage. It is important to detect myocardial fibrosis at an early stage, using non-invasive diagnostic methods. According to the results of echocardiography (ECG), 110 men with general obesity were divided into the following two groups: Group I with epicardial fat thickness (tEAT) ≥ 7 mm (n = 70) and Group II with tEAT < 7 mm (n = 40) without diastolic dysfunction. The levels of metabolic factors, pro-inflammatory cytokines, adipokines, and free fatty acids (FFA), profibrotic markers were determined in both groups. In Group I, the level of interleukin (IL)-6, C-reactive protein, and tumor necrosis factor (TNF)-α increased and that of leptin and adiponectin decreased compared with those in Group II. There was an increase in the level of all studied profibrotic factors in Group I. The level of TNF-α and IL-6 showed a positive correlation with the level of leptin and FFA and a negative correlation with the level of adiponectin. We also observed a relationship between the level of collagen, transforming growth factor (TGF)-β, and metalloproteinase (MMP)-3 and EO. Our results showed that confirmed EO correlates with not only disadipocytosis and increased levels of pro-inflammatory cytokines, but also increased levels of profibrotic factors. This suggests that the studied markers of fibrosis may be used to determine preclinical cardiac fibrosis with lipotoxic myocardial damage in patients with EO.