Decreased KCNE2 Expression Participates in the Development of Cardiac Hypertrophy by Regulation of Calcineurin–NFAT (Nuclear Factor of Activated T Cells) and Mitogen-Activated Protein Kinase Pathways

Liu, Wenjuan; Deng, Jianxin; Ding, Wenwen; Wang, Gang; Shen, Yuanyuan; Zheng, Junmeng; Zhang, Xiaoming; Luo, Yizhi; Lv, Chifei; Wang, Yonghui; Chen, Liqing; Yan, Dewen; Boudreau, Ryan L.; Song, Long‐Sheng; Liu, Jie

doi:10.1161/circheartfailure.117.003960

Cited by 7 publications

(4 citation statements)

References 36 publications

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“…Similar to the results of our pervious [ 10 ] and other studies [ 11 , 12 ], the left ventricular hypertrophy developed on the 4th week after AAC in rats, which was confirmed by pathological observation and atrial natriuretic factor (ANF) mRNA expression in six randomly selected AAC rats. The remaining AAC rats, that is, cardiac hypertrophy rats, were then randomly assigned to three groups ( n = 8 per group), including untreated AAC rats (Model) and AAC rats treated with rutaecarpine 20 or 40 mg/kg/day i.g., respectively.…”

Section: Methodssupporting

confidence: 90%

Rutaecarpine Ameliorates Pressure Overload Cardiac Hypertrophy by Suppression of Calcineurin and Angiotensin II

Huang

Zhou

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Cardiac hypertrophy is a major pathological process to result in heart failure and sudden death. Rutaecarpine, a pentacyclic indolopyridoquinazolinone alkaloid extracted from Evodia rutaecarpa with multiple pharmacological activities, yet the underlying protective effects and the mechanisms on cardiac hypertrophy remain unclear. This study aimed to evaluate the potential effects of rutaecarpine on pressure overload cardiac hypertrophy. Cardiac hypertrophy in rat was developed by abdominal aortic constriction (AAC) for 4 weeks, which was improved by rutaecarpine supplementation (20 or 40 mg/kg/day, i.g.) for another 4 weeks. The level of angiotensin II was increased; the mRNA expression and the activity of calcineurin in the left ventricular tissue were augmented following cardiac hypertrophy. Rutaecarpine administration decreased angiotensin II content and reduced calcineurin expression and activity. Noteworthily, in angiotensin II-induced cardiomyocytes, rutaecarpine ameliorated the hypertrophic effects in a dose-dependent manner and downregulated the increased mRNA expression and activity of calcineurin. In conclusion, rutaecarpine can improve cardiac hypertrophy in pressure overload rats, which may be related to the inhibition of angiotensin II-calcineurin signal pathway.

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Section: Methodssupporting

confidence: 90%

Rutaecarpine Ameliorates Pressure Overload Cardiac Hypertrophy by Suppression of Calcineurin and Angiotensin II

Huang

Zhou

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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“…Previous studies demonstrated that ET-1 plasma levels correlate with the development of cardiac hypertrophy (Liu et al, 2017. In fact, ET-1 has been widely used to induce cardiac remodelling (Archer et al, 2017, Viero et al, 2016 or as a stimulus to study hypertrophy-related pathways (Seidlmayer et al, 2016, Irvine et al, 2013.…”

Section: Endothelin-1 Induced Fetal Gene Expression In Hl-1 Cellsmentioning

confidence: 99%

Endothelial cell modulation of cardiomyocyte gene expression

Jiang

Mohr

Ullrich

et al. 2019

Experimental Cell Research

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WB Western blot WGA Wheat germ agglutinin β-MHC -Myosin heavy chain 2013, Fredriksen et al., 2001). Kidney disease is commonly found in heart failure (HF) patients (Grande et al., 2017). It was found that GFR is associated with the degree of cardiac diastolic dysfunction and adverse clinical outcomes (Jain et al., 2017). A recent nationwide population-based cohort study showed that heart failure patients have a higher risk of developing dementia (Adelborg et al., 2017). Studies also revealed post-mortem that 73.6% ± 7.0% of all cardiomyocytes were mono-nucleated, 25.5% ± 7.4% were bi-nucleated, and 1.0% ± 1.2% were tri-nucleated in the heart of individuals aged one month to 73 years. In agreement with previous studies (Mollova et al., 2013, Olivetti et al., 1996), they established that already 1 month after birth; the final number of cardiomyocytes was reached (3.2 ± 0.75 × 10 9 cells) and remained constant throughout life. By stereological measuring the average volume of cardiomyocytes at different ages, it was found that the adaptive about 3-fold greater (endothelium-derived contracting factors) (Flammer et al., 2012). Furchgott and Zawadzki (Furchgott and Zawadzki, 1980) first described the phenomenon of endothelium-dependent relaxation in 1980. Subsequently, the identification of nitric oxide (NO) as the crucial endothelium-derived mediator of vascular relaxation led to substantial progress in cardiovascular research (Flammer et al., 2012). In addition to with arterial hypertension and echocardiographically documented left ventricular hypertrophy, who received either the AT 1 receptor blocker losartan or the β 1 receptor blocker atenolol, were much less likely to experience such a major cardiovascular event (Kjeldsen et al., 2002). Also whereby NT-proBNP levels are more sensitive and specific to distinguish HF from non-HF subjects (Fonseca et al., 2004). NT-proBNP levels were also suggested to be highly predictive of incident atrial fibrillation, the most common cardiac rhythm abnormality, after adjustment for an extensive number of covariates (Patton et al., 2009). Although ANP and BNP have been recommended to provide prognostic information

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“…The researchers found that, in users who had all three loci mutations of the ABCB1 gene, digoxin was much more highly related to SCD than in people who had no or only 1 T allele (11). Several other genes that are associated with SCD also have been found, such as genes encoding calciumhandling regulating proteins (RyR2, CASQ2, ATP2A2, NOS1AP, TRDN and CALM1) (12)(13)(14)(15)(16)(17), long QT syndrome (KCNJ5, KCNJ2, KCNE2, AKAP9, SNTA1, and AKAP9), idiopathic ventricular fibrillation (DPP6 and KCNJ8), dilated cardiomyopathy (DCM) (NEBL), and hypertrophic cardiomyopathy (HCM) (NEXN) (18,19).…”

Section: Introductionmentioning

confidence: 99%

Identification of genes associated with sudden cardiac death: a network- and pathway-based approach

Wei¹,

Ni²,

Dai³

et al. 2021

J Thorac Dis

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Background: Sudden cardiac death (SCD) accounts for a large proportion of the total deaths across different age groups. Although numerous candidate genes related to SCD have been identified by genetic association studies and genome wide association studies (GWAS), the molecular mechanisms underlying SCD are still unclear, and the biological functions and interactions of these genes remain obscure. To clarify this issue, we performed a comprehensive and systematic analysis of SCD-related genes by a network and pathway-based approach. Methods: By screening the publications deposited in the PubMed and Gene-Cloud Biotechnology Information (GCBI) databases, we collected the genes genetically associated with SCD, which were referred to as the SCD-related gene set (SCDgset). To analyze the biological processes and biochemical pathways of the SCD-related genes, functional analysis was performed. To explore interlinks and interactions of the enriched pathways, pathway crosstalk analysis was implemented. To construct SCD-specific molecular networks, Markov cluster algorithm and Steiner minimal tree algorithm were employed. Results: We collected 257 genes that were reported to be associated with SCD and summarized them in the SCDgset. Most of the biological processes and biochemical pathways were related to heart diseases, while some of the biological functions may be noncardiac causes of SCD. The enriched pathways could be roughly grouped into two modules. One module was related to calcium signaling pathway and the other was related to MAPK pathway. Moreover, two different SCD-specific molecular networks were inferred, and 23 novel genes potentially associated with SCD were also identified.Conclusions: In summary, by means of a network and pathway-based methodology, we explored the pathogenetic mechanism underlying SCD. Our results provide valuable information in understanding the pathogenesis of SCD and include novel biomarkers for diagnosing potential patients with heart diseases; these may help in reducing the corresponding risks and even aid in preventing SCD.

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Decreased KCNE2 Expression Participates in the Development of Cardiac Hypertrophy by Regulation of Calcineurin–NFAT (Nuclear Factor of Activated T Cells) and Mitogen-Activated Protein Kinase Pathways

Cited by 7 publications

References 36 publications

Rutaecarpine Ameliorates Pressure Overload Cardiac Hypertrophy by Suppression of Calcineurin and Angiotensin II

Rutaecarpine Ameliorates Pressure Overload Cardiac Hypertrophy by Suppression of Calcineurin and Angiotensin II

Endothelial cell modulation of cardiomyocyte gene expression

Identification of genes associated with sudden cardiac death: a network- and pathway-based approach

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