Metabolic Alterations in Rat Myocardium in Experimental Acute Atrial Fibrillation

Kondrat'ev, B Y; Ugdyzhekova, D. S.; Антонченко, И. В.; V.V.Aleev,; Попов, С. В.; Афанасьев, С. А.

doi:10.1007/s10517-005-0501-1

Cited by 6 publications

(2 citation statements)

References 7 publications

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“…Indeed, in case of severe long-term tachycardia, energy metabolism of the cells is under stress. 46 In the presence of HF, this is an additional factor negatively affecting mitochondria as main energy factories of the cell. 47,48 Perhaps, when HR is higher than 80 bpm, endogenous stress-limiting mechanisms, associated with hsp60, are close to exhaustion.…”

Section: Discussionmentioning

confidence: 99%

Nonpharmacological Correction of Hypersympatheticotonia in Patients with Chronic Coronary Insufficiency and Severe Left Ventricular Dysfunction

Afanasiev

Павлюкова

Kuzmichkina

et al. 2016

Noninvasive Electrocardiol

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Section: Discussionmentioning

confidence: 99%

Nonpharmacological Correction of Hypersympatheticotonia in Patients with Chronic Coronary Insufficiency and Severe Left Ventricular Dysfunction

Afanasiev

Павлюкова

Kuzmichkina

et al. 2016

Noninvasive Electrocardiol

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“…Furthermore, some biological energy and glucan metabolic process were also found to be related to AF ( Table 2 ). Some studies hypothesized that increased energy requirements in the atria during myocardial fibrillation lead to activation of anaerobic metabolism [ 13 ]. Dong et al found that activation of β3-AR contributes to atrial metabolic remodeling via transcriptional down-regulation of the PGC-1α/NRF-1/Tfam pathway, which is involved in mitochondrial biogenesis and ultimately perturbs mitochondrial function in rapid pacing-induced AF [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Regulatory Network Revealing the Mechanism of Inflammation in Atrial Fibrillation

Zhang

et al. 2015

Med Sci Monit

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BackgroundAtrial fibrillation (AF) is a highly prevalent condition associated with high morbidity and mortality that can cause or exacerbate heart failure and is an important risk factor for stroke. AF is the disorganized propagation of electrical activity in the atrium, which prevents organized contractions. However, the effect of microRNAs and the patterns of the regulatory network of AF remain vague.Material/MethodsThe mRNA expression data of atrial tissue splices from 3 conditions – permanent atrial fibrillation (AF), sinus rhythm (SR), and human left ventricular non-failing myocardium (LV) – were downloaded from GSE2240 and the differentially expressed genes (DEGs) between the 3 kinds of samples were calculated. Then we constructed 3 miRNA-DEGs networks and these networks were integrated to construct the final merged AF-related microRNA regulatory network. Finally, we constructed the miRNA-inflammation networks to detect the roles of miRNAs in inflammation development of AF.ResultsThis network included 108 DEGs, and 27 microRNAs and DEGs are regulated by both microRNAs. We found that a sub-network composed by miR-124, miR-183, miR-215, miR-192, and a DEG of EGR1 were all represents in these 3 networks. Based on functional enrichment analysis, some biological process, such as energy and glucan metabolic process and heart and blood vessel development, were found to be regulated by miRNAs in AF. Some miRNAs, such as miR-26b and miR-355p, were involved in inflammation in AF.ConclusionsIn conclusion, the microRNA regulatory network sheds new light on the molecular mechanism of AF with this non-coding regulated model.

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Dysregulation of insulin-sensitive glucose transporters during insulin resistance-induced atrial fibrillation

Maria

Campolo

Scherlag

et al. 2018

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Diabetes has been identified as major risk factor for atrial fibrillation (AF). Although glucose and insulin disturbances during diabetes may affect atrial function, little is known about the potential pathogenic role of glucose metabolism during AF. Glucose transport into the cell via glucose transporters (GLUTs) is the rate-limiting step of glucose utilization. Although GLUT4 is the major isoform, GLUT8 has emerged as a novel insulin-sensitive cardiac isoform. We hypothesized that atrial glucose homeostasis will be impaired during insulin resistance-induced AF. AF was induced by transesophageal atrial pacing in healthy mice and following a long-term high-fat-diet-induced insulin resistance. Active cell surface GLUT content was measured using the biotinylated photolabeling assay in the intact perfused heart. Atrial fibrosis, advanced glycation end products (AGEs) and glycogen were measured in the atria using histological analyses. Animals fed a high-fat-diet were obese and mildly hyperglycemic, and developed insulin resistance compared to controls. Insulin-resistant (IR) animals demonstrated an increased vulnerability to induced AF, as well as spontaneous AF. Insulin-stimulated translocation of GLUT4 and GLUT8 was down-regulated in the atria of IR animals, as well as their total protein expression. We also reported the absence of fibrosis, glycogen and AGE accumulation in the atria of IR animals. In the absence of structural remodeling and atrial fibrosis, these data suggest that insulin signaling dysregulation, resulting in impaired glucose transport in the atria, could provide a metabolic arrhythmogenic substrate and be a novel early pathogenic factor of AF.

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Metabolic Alterations in Rat Myocardium in Experimental Acute Atrial Fibrillation

Cited by 6 publications

References 7 publications

Nonpharmacological Correction of Hypersympatheticotonia in Patients with Chronic Coronary Insufficiency and Severe Left Ventricular Dysfunction

Nonpharmacological Correction of Hypersympatheticotonia in Patients with Chronic Coronary Insufficiency and Severe Left Ventricular Dysfunction

MicroRNA Regulatory Network Revealing the Mechanism of Inflammation in Atrial Fibrillation

Dysregulation of insulin-sensitive glucose transporters during insulin resistance-induced atrial fibrillation

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