Expression of Sterol Regulatory Element-Binding Proteins in epicardial adipose tissue in patients with coronary artery disease and diabetes mellitus: preliminary study

Pérez‐Belmonte, Luis M.; Moreno-Santos, Inmaculada; Cabrera-Bueno, Fernando; Sánchez-Espín, Gemma; Castellano, Daniel; Such, Miguel; Crespo-Leiro, María G.; Carrasco-Chinchilla, Fernando; Alonso‐Pulpón, Luis; López-Garrido, Miguel A.; Ruíz-Salas, Amalio; Becerra-Muñoz, Víctor Manuel; Gómez‐Doblas, Juan José; Teresa–Galván, Eduardo de; Jiménez-Navarro, Manuel F.

doi:10.7150/ijms.17821

Cited by 15 publications

(15 citation statements)

References 26 publications

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“…EAT represents a visceral brown-like adipose tissue located between the myocardium and the inner layer of visceral pericardium with a close anatomical proximity to the myocardium 4 . A functional EAT has been proposed to play a protector role over the myocardium but in pathological situations may be implicated in the development and/or progression of heart disease 3 - 5 . Several studies have shown that EAT is associated with the pathogenesis of HF, but focusing on EAT volume determined by echocardiography, magnetic resonance or computed tomography.…”

Section: Discussionmentioning

confidence: 99%

Expression of epicardial adipose tissue thermogenic genes in patients with reduced and preserved ejection fraction heart failure

Pérez‐Belmonte¹,

Moreno-Santos²,

Gómez‐Doblas³

et al. 2017

Int. J. Med. Sci.

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Epicardial adipose tissue has been proposed to participate in the pathogenesis of heart failure. The aim of our study was to assess the expression of thermogenic genes (Uncoupling protein 1 (UCP1), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), and PR-domain-missing 16 (PRDM16) in epicardial adipose tissue in patients with heart failure, stablishing the difference according to left ventricular ejection fraction (reduced or preserved). Among the 75 patients in our study, 42.7% (n=32) had reduced left ventricular ejection fraction. UCP1, PGC1α and PRDM16 mRNA in EAT were significantly lower in patients with reduced left ventricular ejection fraction. Multiple regression analysis showed that age, male gender, body max index, presence of obesity, type-2-diabetes mellitus, hypertension and coronary artery disease and left ventricular ejection fraction were associated with the expression levels of UCP1, PGC1α and PRDM16 mRNA. Thermogenic genes expressions in epicardial adipose tissue (UCP1: OR 0.617, 95%CI 0.103-0.989, p=0.042; PGC1α: OR 0.416, 95%CI 0.171-0.912, p=0.031; PRDM16: OR 0.643, 95%CI 0.116-0.997, p=0.044) were showed as protective factors against the presence of heart failure with reduced left ventricular ejection fraction, and age (OR 1.643, 95%CI 1.001-3.143, p=0.026), presence of coronary artery disease (OR 6.743, 95%CI 1.932-15.301, p<0.001) and type-2-diabetes mellitus (OR 4.031, 95%CI 1.099-7.231, p<0.001) were associated as risk factors. The adequate expression of thermogenic genes has been shown as possible protective factors against heart failure with reduced ejection fraction, suggesting that a loss of functional epicardial adipose tissue brown-like features would participate in a deleterious manner on heart metabolism. Thermogenic genes could represent a future novel therapeutic target in heart failure.

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Section: Discussionmentioning

confidence: 99%

Expression of epicardial adipose tissue thermogenic genes in patients with reduced and preserved ejection fraction heart failure

Pérez‐Belmonte¹,

Moreno-Santos²,

Gómez‐Doblas³

et al. 2017

Int. J. Med. Sci.

Self Cite

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“…Silencing of mirna-122 leads to a decrease in total cholesterol and triglyceride in plasma (49). at present, lncrnas have emerged as critical factors in the promotion of hepatic gluconeogenesis and cholesterol biosynthesis via the SreBP pathway (46). However, their functions in cad remain unknown, which highlights the importance of the results of the present study.…”

Section: Discussionmentioning

confidence: 64%

“…Increasing studies have focused on the correlation between SREBP and cad. SreBP is upregulated in patients with cad and is a cardiovascular risk factor for the severity of cad and poor lipid control (46). Another study identified that the recessive allele (TT vs. CT+CC) of SREBP1 rs9902941 is highly expressed in patients with cad compared with the normal control (47).…”

Section: Discussionmentioning

confidence: 99%

A novel plasma lncRNA ENST00000416361 is upregulated in coronary artery disease and is related to inflammation and lipid metabolism

Yan

et al. 2020

Mol Med Report

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coronary artery disease (cad) is a serious threat to human health and a major cause of mortality worldwide. long noncoding rnas (lncrnas) affect the occurrence and development of cad via the regulation of cell proliferation and apoptosis, inflammatory responses and lipid metabolism. Screening methods and therapeutic strategies for cad have been extensively studied. The present study analyzed clinical indexes of 187 patients with CAD and 150 healthy subjects. The data showed significant differences in diabetes mellitus, hypertension, high-density lipoprotein level and smoking history between the CAD group and the control group. A series of differentially expressed lncRNAs were detected in the plasma samples of three patients with CAD by high-throughput sequencing. reverse transcription-quantitative (rT-q)Pcr data revealed that the expression level of the novel lncRNA enST00000416361 was ~2.3-fold higher in the plasma of 50 patients with CAD compared with the 50 control subjects. receiver operating characteristic (roc) curves were generated, and the area under the roc curve was 0.7902. Knockdown of ENST00000416361 in human umbilical vein endothelial cells markedly downregulated interleukin-6 and tumor necrosis factor-α levels. In addition, sterol regulatory element binding transcription factor (SreBP)1 and SreBP2 were upregulated in patients with cad, and they were positively correlated with the expression of ENST00000416361. RT-qPCR further demonstrated that knockdown of enST00000416361 led to the downregulation of SreBP1 and SreBP2. overall, the novel lncRNA ENST00000416361 may be associated with CAD-induced inflammation and lipid metabolism, and it may serve as a potential biomarker for CAD.

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“…Interestingly, high levels of myocardial SREBP1 have been reported in patients with pressure overloaded heart and metabolic syndrome [50] and might be causally related to selective insulin resistance and inhibition of uncoupling protein 3 (UCP3) expression in the mouse heart [51]. Besides, the high expression of both SREBP1 and SREBP2 mRNA in epicardial adipose tissue has been identified as a cardiovascular risk factor in patients with type-2 diabetes [52]. Myocardial SREBP1c is also involved in the regulation of cardiac parasympathetic response [11].…”

Section: Discussionmentioning

confidence: 99%

Modulation of Fatty Acid-Related Genes in the Response of H9c2 Cardiac Cells to Palmitate and n-3 Polyunsaturated Fatty Acids

Cetrullo

D’Adamo

Panichi

et al. 2020

Cells

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While high levels of saturated fatty acids are associated with impairment of cardiovascular functions, n-3 polyunsaturated fatty acids (PUFAs) have been shown to exert protective effects. However the molecular mechanisms underlying this evidence are not completely understood. In the present study we have used rat H9c2 ventricular cardiomyoblasts as a cellular model of lipotoxicity to highlight the effects of palmitate, a saturated fatty acid, on genetic and epigenetic modulation of fatty acid metabolism and fate, and the ability of PUFAs, eicosapentaenoic acid, and docosahexaenoic acid, to contrast the actions that may contribute to cardiac dysfunction and remodeling. Treatment with a high dose of palmitate provoked mitochondrial depolarization, apoptosis, and hypertrophy of cardiomyoblasts. Palmitate also enhanced the mRNA levels of sterol regulatory element-binding proteins (SREBPs), a family of master transcription factors for lipogenesis, and it favored the expression of genes encoding key enzymes that metabolically activate palmitate and commit it to biosynthetic pathways. Moreover, miR-33a, a highly conserved microRNA embedded in an intronic sequence of the SREBP2 gene, was co-expressed with the SREBP2 messenger, while its target carnitine palmitoyltransferase-1b was down-regulated. Manipulation of the levels of miR-33a and SREBPs allowed us to understand their involvement in cell death and hypertrophy. The simultaneous addition of PUFAs prevented the effects of palmitate and protected H9c2 cells. These results may have implications for the control of cardiac metabolism and dysfunction, particularly in relation to dietary habits and the quality of fatty acid intake.

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Expression of Sterol Regulatory Element-Binding Proteins in epicardial adipose tissue in patients with coronary artery disease and diabetes mellitus: preliminary study

Cited by 15 publications

References 26 publications

Expression of epicardial adipose tissue thermogenic genes in patients with reduced and preserved ejection fraction heart failure

Expression of epicardial adipose tissue thermogenic genes in patients with reduced and preserved ejection fraction heart failure

A novel plasma lncRNA ENST00000416361 is upregulated in coronary artery disease and is related to inflammation and lipid metabolism

Modulation of Fatty Acid-Related Genes in the Response of H9c2 Cardiac Cells to Palmitate and n-3 Polyunsaturated Fatty Acids

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