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Regulation of DNA methylation and 2-OG/TET signaling by choline alleviated cardiac hypertrophy in spontaneously hypertensive rats. PubMed SCIE
期刊论文 | 2019 , 128 , 26-37 | Journal of molecular and cellular cardiology
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Abstract :

DNA methylation is a well-defined epigenetic modification that regulates gene transcription. However, the role of DNA methylation in the cardiac hypertrophy seen in hypertension is unclear. This study was performed to investigate genome-wide DNA methylation profiles in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto rats (WKY), and the cardioprotective effect of choline. Eight-week-old male SHRs received intraperitoneal injections of choline (8 mg/kg/day) for 8 weeks. SHRs showed aberrant methylation distribution on chromosomes and genome regions, with decreased methylation levels at CHG and CHH sites. A total of 91,559 differentially methylated regions (DMRs) were detected between SHRs and WKY rats, of which 28,197 were demethylated and 63,362 were methylated. Choline treatment partly restored the DMRs in SHRs, which were related to 131 genes. Gene ontology analysis and Kyoto Encyclopedia of Genes and Genomes analysis of DMRs suggested that choline partly reversed the dysfunctions of biological processes, cellular components and molecular functions in SHRs. Moreover, the inhibition of 2-oxoglutarate accumulation by choline, thereby inhibiting excessive activation of ten-eleven translocation methylcytosine dioxygenase enzymes, may correlate with the beneficial effects of choline on methylation levels, cardiac hypertrophy and cardiac function of SHRs, as indicated by decreased heart rate and blood pressure, and increased ejection fraction and fractional shortening. This study provides the first genome-wide DNA methylation profile of the hypertrophic myocardium of SHRs and suggests a novel role for this epigenetic modification in hypertension. Choline treatment may represent a promising approach for modification of DNA methylation and optimization of the epigenetic profile for antihypertensive therapy.

Keyword :

DNA methylation Cardiac hypertrophy 2-oxoglutarate Hypertension Choline Spontaneously hypertensive rat

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GB/T 7714 Liu Longzhu , He Xi , Zhao Ming et al. Regulation of DNA methylation and 2-OG/TET signaling by choline alleviated cardiac hypertrophy in spontaneously hypertensive rats. [J]. | Journal of molecular and cellular cardiology , 2019 , 128 : 26-37 .
MLA Liu Longzhu et al. "Regulation of DNA methylation and 2-OG/TET signaling by choline alleviated cardiac hypertrophy in spontaneously hypertensive rats." . | Journal of molecular and cellular cardiology 128 (2019) : 26-37 .
APA Liu Longzhu , He Xi , Zhao Ming , Yang Si , Wang Shengpeng , Yu Xiaojiang et al. Regulation of DNA methylation and 2-OG/TET signaling by choline alleviated cardiac hypertrophy in spontaneously hypertensive rats. . | Journal of molecular and cellular cardiology , 2019 , 128 , 26-37 .
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Cholinergic drugs ameliorate endothelial dysfunction by decreasing O-GlcNAcylation via M3 AChR-AMPK-ER stress signaling SCIE
期刊论文 | 2019 , 222 , 1-12 | LIFE SCIENCES
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Aims: Obesity is associated with increased cardiovascular morbidity and mortality. It is accompanied by augmented O-linked beta-N-acetylglucosamine (O-GlcNAc) modification of proteins via increasing hexosamine bio-synthetic pathway (HBP) flux. However, the changes and regulation of the O-GlcNAc levels induced by obesity are unclear. Main methods: High fat diet (HFD) model was induced obesity in mice with or without the cholinergic drug pyridostigmine (PYR, 3 mg/kg/d) for 22 weeks and in vitro human umbilical vein endothelial cells (HUVECs) was treated with high glucose (HG, 30 mM) with or without acetylcholine (ACh). Key findings: PYR significantly reduced body weight, blood glucose, and O-GlcNAcylation levels and attenuated vascular endothelial cells detachment in HFD-fed mice. HG addition induced endoplasmic reticulum (ER) stress and increased O-GlcNAcylation levels and apoptosis in HUVECs in a time-dependent manner. Additionally, HG decreased levels of phosphorylated AMP-activated protein kinase (AMPK). Interestingly, ACh significantly blocked damage to HUVECs induced by HG. Furthermore, the effects of ACh on HG-induced ER stress, O-GlcNAcylation, and apoptosis were prevented by treating HUVECs with 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP, a selective M3 AChR antagonist) or compound C (Comp C, an AMPK inhibitor). Treatment with 5-aminoimidazole-4-carboxamide ribose (AICAR, an AMPK activator), 4-phenyl butyric acid (4-PBA, an ER stress inhibitor), and 6-diazo-5-oxonorleucine (DON, a GFAT antagonist) reproduced a similar effect with ACh. Significance: Activation of cholinergic signaling ameliorated endothelium damage, reduced levels of ER stress, O-GlcNAcylation, and apoptosis in mice and HUVECs under obese conditions, which may function through M3 AChR-AMPK signaling.

Keyword :

O-GlcNAc Endothelial cell apoptosis Cholinergic drugs M3 AChR-AMPK Obesity ER stress

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GB/T 7714 Cui, Yan-Ling , Xue, Run-Qing , He, Xi et al. Cholinergic drugs ameliorate endothelial dysfunction by decreasing O-GlcNAcylation via M3 AChR-AMPK-ER stress signaling [J]. | LIFE SCIENCES , 2019 , 222 : 1-12 .
MLA Cui, Yan-Ling et al. "Cholinergic drugs ameliorate endothelial dysfunction by decreasing O-GlcNAcylation via M3 AChR-AMPK-ER stress signaling" . | LIFE SCIENCES 222 (2019) : 1-12 .
APA Cui, Yan-Ling , Xue, Run-Qing , He, Xi , Zhao, Ming , Yu, Xiao-Jiang , Liu, Long-Zhu et al. Cholinergic drugs ameliorate endothelial dysfunction by decreasing O-GlcNAcylation via M3 AChR-AMPK-ER stress signaling . | LIFE SCIENCES , 2019 , 222 , 1-12 .
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Pyridostigmine alleviates cardiac dysfunction via improving mitochondrial cristae shape in a mouse model of metabolic syndrome. PubMed
期刊论文 | 2019 , 134 , 119-132 | Free radical biology & medicine
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Insulin resistance and autonomic imbalance are important pathological processes in metabolic syndrome-induced cardiac remodeling. Recent studies determined that disruption of mitochondrial cristae shape is associated with myocardial ischemia; however, the change in cristae shape in metabolic syndrome-induced cardiac remodeling remains unclear. This study determined the effect of pyridostigmine (PYR), which reversibly inhibits cholinesterase to improve autonomic imbalance, on high-fat diet (HFD)-induced cardiac insulin resistance and explored the potential effect on the shape of mitochondrial cristae. Feeding of a HFD for 22 weeks led to an irregular and even lysed cristae structure in cardiac mitochondria, which contributed to decreased mitochondrial content and ATP production and increased oxygen species production, ultimately impairing insulin signaling and lipid metabolism. Interestingly, PYR enhanced vagal activity by increasing acetylcholine production and exerted mito-protective effects by activating the LKB1/AMPK/ACC signal pathway. Specifically, PYR upregulated OPA1 and Mfn1/2 expression, promoted the formation of the mitofilin/CHCHD3/Sam50 complex, and decreased p-Drp1 and Fis1 expression, resulting in tight and parallel cristae and increasing cardiac mitochondrial complex subunit expression and ATP generation as well as decreasing release of cytochrome C from mitochondria and oxidative damage. Furthermore, PYR improved glucose and insulin tolerance and insulin-stimulated Akt phosphorylation, decreased lipid toxicity, and ultimately ameliorated HFD-induced cardiac remodeling and dysfunction. In conclusion, PYR prevented cardiac and insulin insensitivity and remodeling by stimulating vagal activity to regulate mitochondrial cristae shape and function in HFD-induced metabolic syndrome in mice. These results provide novel insights for the development of a therapeutic strategy for obesity-induced cardiac dysfunction that targets mitochondrial cristae.

Keyword :

Mitochondrial cristae shape Cardiac dysfunction Metabolic syndrome Pyridostigmine

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GB/T 7714 Xue Run-Qing , Yu Xiao-Jiang , Zhao Ming et al. Pyridostigmine alleviates cardiac dysfunction via improving mitochondrial cristae shape in a mouse model of metabolic syndrome. [J]. | Free radical biology & medicine , 2019 , 134 : 119-132 .
MLA Xue Run-Qing et al. "Pyridostigmine alleviates cardiac dysfunction via improving mitochondrial cristae shape in a mouse model of metabolic syndrome." . | Free radical biology & medicine 134 (2019) : 119-132 .
APA Xue Run-Qing , Yu Xiao-Jiang , Zhao Ming , Xu Man , Wu Qing , Cui Yan-Ling et al. Pyridostigmine alleviates cardiac dysfunction via improving mitochondrial cristae shape in a mouse model of metabolic syndrome. . | Free radical biology & medicine , 2019 , 134 , 119-132 .
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Pharmacological Modulation of Vagal Nerve Activity in Cardiovascular Diseases. PubMed Scopus CSCD SCIE
期刊论文 | 2019 , 35 (1) , 156-166 | Neuroscience bulletin
WoS CC Cited Count: 2 SCOPUS Cited Count: 2
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Cardiovascular diseases are life-threatening illnesses with high morbidity and mortality. Suppressed vagal (parasympathetic) activity and increased sympathetic activity are involved in these diseases. Currently, pharmacological interventions primarily aim to inhibit over-excitation of sympathetic nerves, while vagal modulation has been largely neglected. Many studies have demonstrated that increased vagal activity reduces cardiovascular risk factors in both animal models and human patients. Therefore, the improvement of vagal activity may be an alternate approach for the treatment of cardiovascular diseases. However, drugs used for vagus nerve activation in cardiovascular diseases are limited in the clinic. In this review, we provide an overview of the potential drug targets for modulating vagal nerve activation, including muscarinic, and β-adrenergic receptors. In addition, vagomimetic drugs (such as choline, acetylcholine, and pyridostigmine) and the mechanism underlying their cardiovascular protective effects are also discussed.

Keyword :

Cholinergic drugs Muscarinic receptor Cardiovascular disease Vagomimetic drugs α7-nACh receptor Vagus nerve

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GB/T 7714 Liu Longzhu , Zhao Ming , Yu Xiaojiang et al. Pharmacological Modulation of Vagal Nerve Activity in Cardiovascular Diseases. [J]. | Neuroscience bulletin , 2019 , 35 (1) : 156-166 .
MLA Liu Longzhu et al. "Pharmacological Modulation of Vagal Nerve Activity in Cardiovascular Diseases." . | Neuroscience bulletin 35 . 1 (2019) : 156-166 .
APA Liu Longzhu , Zhao Ming , Yu Xiaojiang , Zang Weijin . Pharmacological Modulation of Vagal Nerve Activity in Cardiovascular Diseases. . | Neuroscience bulletin , 2019 , 35 (1) , 156-166 .
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Choline ameliorates cardiac hypertrophy by regulating metabolic remodelling and UPRmt through SIRT3-AMPK pathway. PubMed SCIE
期刊论文 | 2019 , 115 (3) , 530-545 | Cardiovascular research
WoS CC Cited Count: 2
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Cardiac hypertrophy is characterised by a shift in metabolic substrate utilisation, but the molecular events underlying the metabolic remodelling remain poorly understood. We explored metabolic remodelling and mitochondrial dysfunction in cardiac hypertrophy and investigated the cardioprotective effects of choline.The experiments were conducted using a model of ventricular hypertrophy by partially banding the abdominal aorta of Sprague Dawley rats. Cardiomyocyte size and cardiac fibrosis were significantly increased in hypertrophic hearts. In vitro cardiomyocyte hypertrophy was induced by exposing neonatal rat cardiomyocytes to angiotensin II (Ang II) (10-6 M, 24 h). Choline attenuated the mito-nuclear protein imbalance and activated the mitochondrial unfolded protein response (UPRmt) in the heart, thereby preserving the ultrastructure and function of mitochondria in the context of cardiac hypertrophy. Moreover, choline inhibited myocardial metabolic dysfunction by promoting the expression of proteins involved in ketone body and fatty acid metabolism in response to pressure overload, accompanied by the activation of sirtuin 3/AMP-activated protein kinase (SIRT3-AMPK) signalling. In vitro analyses demonstrated that SIRT3 siRNA diminished choline-mediated activation of ketone body metabolism and UPRmt, as well as inhibition of hypertrophic signals. Intriguingly, serum from choline-treated abdominal aorta banding models (where β-hydroxybutyrate was increased) attenuated Ang II-induced myocyte hypertrophy, which indicates that β-hydroxybutyrate is important for the cardioprotective effects of choline.Choline attenuated cardiac dysfunction by modulating the expression of proteins involved in ketone body and fatty acid metabolism, and induction of UPRmt; this was likely mediated by activation of the SIRT3-AMPK pathway. Taken together, these results identify SIRT3-AMPK as a key cardiac transcriptional regulator that helps orchestrate an adaptive metabolic response to cardiac stress. Choline treatment may represent a new therapeutic strategy for optimising myocardial metabolism in the context of hypertrophy and heart failure.

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GB/T 7714 Xu Man , Xue Run-Qing , Lu Yi et al. Choline ameliorates cardiac hypertrophy by regulating metabolic remodelling and UPRmt through SIRT3-AMPK pathway. [J]. | Cardiovascular research , 2019 , 115 (3) : 530-545 .
MLA Xu Man et al. "Choline ameliorates cardiac hypertrophy by regulating metabolic remodelling and UPRmt through SIRT3-AMPK pathway." . | Cardiovascular research 115 . 3 (2019) : 530-545 .
APA Xu Man , Xue Run-Qing , Lu Yi , Yong Su-Yun , Wu Qing , Cui Yan-Ling et al. Choline ameliorates cardiac hypertrophy by regulating metabolic remodelling and UPRmt through SIRT3-AMPK pathway. . | Cardiovascular research , 2019 , 115 (3) , 530-545 .
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Egr-1 mediates leptin-induced PPAR gamma reduction and proliferation of pulmonary artery smooth muscle cells SCIE PubMed Scopus
期刊论文 | 2018 , 29 (3) , 356-362 | MOLECULAR BIOLOGY OF THE CELL
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Loss of peroxisome proliferator-activated receptor gamma (PPAR gamma) has been found to contribute to pulmonary artery smooth muscle cell (PASMC) proliferation and pulmonary arterial remodeling therefore the development of pulmonary hypertension (PH). Yet, the molecular mechanisms underlying PPAR gamma reduction in PASMC remain poorly understood. Here, we demonstrated that leptin dose- and time-dependently inducued PPAR gamma down-regulation and proliferation of primary cultured rat PASMC, this was accompanied with the activation of extracellular regulated kinase1/2 (ERK1/2) signaling pathway and subsequent induction of early growth response-1 (Egr-1) expression. The presence of MEK inhibitors U0126 or PD98059, or prior silencing Egr-1 with small interfering RNA suppressed leptin-induced PPAR gamma reduction. In addition, activation of PPAR gamma by pioglitazone or targeting ERK1/2/Egr-1 suppressed leptin-induced PASMC proliferation. Taken together, our study indicates that ERK1/2 signaling pathway-mediated leptin-induced PPAR gamma reduction and PASMC proliferation through up-regulation of Egr-1 and suggests that targeting leptin/ERK1/2/Egr-1 pathway might have potential value in ameliorating vascular remodeling and benefit PH.

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GB/T 7714 Xie, Xinming , Li, Shaojun , Zhu, Yanting et al. Egr-1 mediates leptin-induced PPAR gamma reduction and proliferation of pulmonary artery smooth muscle cells [J]. | MOLECULAR BIOLOGY OF THE CELL , 2018 , 29 (3) : 356-362 .
MLA Xie, Xinming et al. "Egr-1 mediates leptin-induced PPAR gamma reduction and proliferation of pulmonary artery smooth muscle cells" . | MOLECULAR BIOLOGY OF THE CELL 29 . 3 (2018) : 356-362 .
APA Xie, Xinming , Li, Shaojun , Zhu, Yanting , Liu, Lu , Ke, Rui , Wang, Jian et al. Egr-1 mediates leptin-induced PPAR gamma reduction and proliferation of pulmonary artery smooth muscle cells . | MOLECULAR BIOLOGY OF THE CELL , 2018 , 29 (3) , 356-362 .
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Identification of atrial fibrillation-associated microRNAs in left and right atria of rheumatic mitral valve disease patients. PubMed
期刊论文 | 2018 | Genes & genetic systems
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MicroRNA (miRNA) is associated with the development and pathology of atrial fibrillation (AF). In this study, we performed miRNA profiling of left and right atrium samples from individuals with AF-associated rheumatic mitral valve disease (RMVD) to identify miRNAs that are differentially expressed between RMVD patients with AF and RMVD with sinus rhythm (SR) as controls, as well as between left and right atrium samples from RMVD with AF patients. We performed hematoxylin and eosin staining as well as scanning and transmission electron microscopy to examine in detail any morphological and physiological changes in cardiomyocytes from RMVD patients with AF or SR. Raman spectroscopy was performed to identify molecular and structural information of left and right atrium samples from RMVD with AF and SR. We also performed miRNA array profiling to separately profile miRNA expression patterns of right and left atrium samples from three independent RMVD patients with AF and in a mixed pool of 10 RMVD patients with SR. Morphological and physiological analysis showed distinct shapes and structures of cardiomyocytes from the left and right atria of RMVD patients with AF or SR. The intensity of Raman spectroscopy of atrial tissues from RMVD patients with AF and with SR was different. miRNA profiling showed differential miRNA expression between RMVD patients with AF or SR, and between the left and right atria of RMVD patients with AF. Importantly, miRNAs showed consistent expression changes among all three patients, suggesting that these miRNAs have potential as markers for AF pathology. Our results revealed potential biomarker miRNAs for atrial fibrillation pathology in patients with RMVD. Meanwhile, our data suggested that miR-10b and miR-138-2, which were both significantly increased in the left atrium, are responsible for morphological and physiological phenotype differences between the left and right atria.

Keyword :

atrial fibrillation rheumatic mitral valve disease biomarker microRNA

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GB/T 7714 Yan Yang , Shi Rui , Yu Xiaojiang et al. Identification of atrial fibrillation-associated microRNAs in left and right atria of rheumatic mitral valve disease patients. [J]. | Genes & genetic systems , 2018 .
MLA Yan Yang et al. "Identification of atrial fibrillation-associated microRNAs in left and right atria of rheumatic mitral valve disease patients." . | Genes & genetic systems (2018) .
APA Yan Yang , Shi Rui , Yu Xiaojiang , Sun Chaofeng , Zang Weijin , Tian Hongyan . Identification of atrial fibrillation-associated microRNAs in left and right atria of rheumatic mitral valve disease patients. . | Genes & genetic systems , 2018 .
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Hypoxia selectively upregulates cation channels and increases cytosolic [Ca2+] in pulmonary, but not coronary, arterial smooth muscle cells SCIE PubMed Scopus
期刊论文 | 2018 , 314 (4) , C504-C517 | AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
WoS CC Cited Count: 6 SCOPUS Cited Count: 5
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Ca2+ signaling, particularly the mechanism via store-operated Ca2+ entry (SOCE) and receptor-operated Ca2+ entry (ROCE). plays a critical role in the development of acute hypoxia-induced pulmonary vasoconstriction and chronic hypoxia-induced pulmonary hypertension. This study aimed to test the hypothesis that chronic hypoxia differentially regulates the expression of proteins that mediate SOCK and ROCK [stromal interacting molecule (STIM). Orai, and canonical transient receptor potential channel TRPC6] in pulmonary (PASMC) and coronary (CASMC) artery smooth muscle cells. The resting cytosolic [Ca2+] ([Ca-2+](c)yt) and the stored [Ca2+] in the sarcoplasmic reticulum were not different in CASMC and PASMC. Seahorse measurement showed a similar level of mitochondrial bioenergetics (basal respiration and ATP production) between CASMC and PASMC. Glycolysis was significantly higher in PASMC than in CASMC. The amplitudes of cyclopiazonic acid-induced SOCE and OAG-induced ROCE in CASMC are slightly, but significantly, greater than in PASMC. The frequency and the area under the curve of Ca2+ oscillations induced by ATP and histamine were also larger in CASMC than in PASMC. Na+/Ca2+ exchanger-mediated increases in [Ca2+](cyt) did not differ significantly between CASMC and PASMC. The basal protein expression levels of STIM1/2. Orai1/2, and TRPC6 were higher in CASMC than in PASMC, but hypoxia (3% O-2 for 72 h) significantly upregulated protein expression levels of STIM1/STIM2, Orai1/Orai2, and TRPC6 and increased the resting [Ca2+](cyt) only in PASMC, but not in CASMC. The different response of essential components of store-operated and receptoroperated Ca2+ channels to hypoxia is a unique intrinsic property of PASMC, which is likely one of the important explanations why hypoxia causes pulmonary vasoconstriction and induces pulmonary vascular remodeling, but causes coronary vasodilation.

Keyword :

hypoxia coronary vasodilation hypoxic pulmonary vasoconstriction calcium signaling

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GB/T 7714 He, Xi , Song, Shanshan , Ayon, Ramon J. et al. Hypoxia selectively upregulates cation channels and increases cytosolic [Ca2+] in pulmonary, but not coronary, arterial smooth muscle cells [J]. | AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY , 2018 , 314 (4) : C504-C517 .
MLA He, Xi et al. "Hypoxia selectively upregulates cation channels and increases cytosolic [Ca2+] in pulmonary, but not coronary, arterial smooth muscle cells" . | AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY 314 . 4 (2018) : C504-C517 .
APA He, Xi , Song, Shanshan , Ayon, Ramon J. , Balisterieri, Angela , Black, Stephen M. , Makino, Ayako et al. Hypoxia selectively upregulates cation channels and increases cytosolic [Ca2+] in pulmonary, but not coronary, arterial smooth muscle cells . | AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY , 2018 , 314 (4) , C504-C517 .
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Pyridostigmine protects against cardiomyopathy associated with adipose tissue browning and improvement of vagal activity in high-fat diet rats SCIE PubMed Scopus
期刊论文 | 2018 , 1864 (4) , 1037-1050 | BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
WoS CC Cited Count: 7 SCOPUS Cited Count: 8
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Obesity, a major contributor to the development of cardiovascular diseases, is associated with an autonomic imbalance characterized by sympathetic hyperactivity and diminished vagal activity. Vagal activation plays important roles in weight loss and improvement of cardiac function. Pyridostigmine is a reversible acetylcholinesterase inhibitor, but whether it ameliorates cardiac lipid accumulation and cardiac remodeling in rats fed a high-fat diet has not been determined. This study investigated the effects of pyridostigmine on high-fat diet induced cardiac dysfunction and explored the potential mechanisms. Rats were fed a normal or high-fat diet and treated with pyridostigmine. Vagal discharge was evaluated using the BL-420S system, and cardiac function by echocardiograms. Lipid deposition and cardiac remodeling were determined histologically. Lipid utility was assessed by qPCR. A high-fat diet led to a significant reduction in vagal discharge and lipid utility and a marked increase in lipid accumulation, cardiac remodeling, and cardiac dysfunction. Pyridostigmine improved vagal activity and lipid metabolism disorder and cardiac remodeling, accompanied by an improvement of cardiac function in high-fat diet-fed rats. An increase in the browning of white adipose tissue in pyridostigmine-treated rats was also observed and linked to the expression of UCP-1 and CIDEA. Additionally, pyridostigmine facilitated activation of brown adipose tissue via activation of the SIRT-1/AMPK/PGC-l alpha pathway. In conclusion, a high-fat diet resulted in cardiac lipid accumulation, cardiac remodeling, and a significant decrease in vagal discharge. Pyridostigmine ameliorated cardiomyopathy, an effect related to reduced cardiac lipid accumulation, and facilitated the browning of white adipose tissue while activating brown adipose tissue.

Keyword :

Obesity Adipose tissue Cardiac remodeling Cardiac lipid accumulation Pyridostigmine

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GB/T 7714 Lu, Yi , Wu, Qing , Liu, Long-Zhu et al. Pyridostigmine protects against cardiomyopathy associated with adipose tissue browning and improvement of vagal activity in high-fat diet rats [J]. | BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE , 2018 , 1864 (4) : 1037-1050 .
MLA Lu, Yi et al. "Pyridostigmine protects against cardiomyopathy associated with adipose tissue browning and improvement of vagal activity in high-fat diet rats" . | BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE 1864 . 4 (2018) : 1037-1050 .
APA Lu, Yi , Wu, Qing , Liu, Long-Zhu , Yu, Xiao-Jiang , Liu, Jin-Jun , Li, Man-Xiang et al. Pyridostigmine protects against cardiomyopathy associated with adipose tissue browning and improvement of vagal activity in high-fat diet rats . | BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE , 2018 , 1864 (4) , 1037-1050 .
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Recent progress of mitochondrial quality control in ischemic heart disease and its role in cardio-protection of vagal nerve]. PubMed Scopus CSCD PKU
期刊论文 | 2017 , 69 (5) , 579-586 | Sheng li xue bao : [Acta physiologica Sinica]
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Ischemic heart disease (IHD) is the life-threatening cardiovascular disease. Mitochondria have emerged as key participants and regulators of cellular energy demands and signal transduction. Mitochondrial quality is controlled by a number of coordinated mechanisms including mitochondrial fission, fusion and mitophagy, which plays an important role in maintaining healthy mitochondria and cardiac function. Recently, dysfunction of each process in mitochondrial quality control has been observed in the ischemic hearts. This review describes the mechanism of mitochondrial dynamics and mitophagy as well as its performance linked to myocardial ischemia. Moreover, in combination with our study, we will discuss the effect of vagal nerve on mitochondria in cardio-protection.

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GB/T 7714 Xue Run-Qing , Xu Man , Yu Xiao-Jiang et al. Recent progress of mitochondrial quality control in ischemic heart disease and its role in cardio-protection of vagal nerve]. [J]. | Sheng li xue bao : [Acta physiologica Sinica] , 2017 , 69 (5) : 579-586 .
MLA Xue Run-Qing et al. "Recent progress of mitochondrial quality control in ischemic heart disease and its role in cardio-protection of vagal nerve]." . | Sheng li xue bao : [Acta physiologica Sinica] 69 . 5 (2017) : 579-586 .
APA Xue Run-Qing , Xu Man , Yu Xiao-Jiang , Liu Long-Zhu , Zang Wei-Jin . Recent progress of mitochondrial quality control in ischemic heart disease and its role in cardio-protection of vagal nerve]. . | Sheng li xue bao : [Acta physiologica Sinica] , 2017 , 69 (5) , 579-586 .
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