Atrial remodeling in atrial fibrillation and association between microRNA network and atrial fibrillation

Zhang, Ying; Dong, De-Li; Yang, Baofeng

doi:10.1007/s11427-011-4241-3

Cited by 20 publications

(6 citation statements)

References 39 publications

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“…Electrical and structural remodeling constitutes the main pathophysiological mechanisms responsible for development of AF, which is initiated and maintained by focal ectopic firing, re-entry circuits, or both conditions simultaneously (209). Furthermore, abnormal Ca 2+ dynamics and neurohormonal dysregulation take part in the making of the conduction disorder (210).…”

Section: Mirna In Atrial Fibrillationmentioning

confidence: 99%

microRNA in Cardiovascular Aging and Age-Related Cardiovascular Diseases

Lucia

Komici²,

Borghetti

et al. 2017

Front. Med.

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Over the last decades, life expectancy has significantly increased although several chronic diseases persist in the population, with aging as the leading risk factor. Despite improvements in diagnosis and treatment, many elderlies suffer from cardiovascular problems that are much more frequent in an older, more fragile organism. In the long term, age-related cardiovascular diseases (CVDs) contribute to the decline of quality of life and ability to perform normal activities of daily living. microRNAs (miRNAs) are a class of small non-coding RNAs that regulate gene expression at the posttranscriptional level in both physiological and pathological conditions. In this review, we will focus on the role of miRNAs in aging and age-related CVDs as heart failure, hypertension, atherosclerosis, atrial fibrillation, and diabetes mellitus. miRNAs are key regulators of complex biological mechanisms, representing an exciting potential therapeutic target in CVDs. Moreover, one major challenge in geriatric medicine is to find reliable biomarkers for diagnosis, prognosis, and prediction of the response to specific drugs. miRNAs represent a very promising tool due to their stability in the circulation and unique signature in CVDs. However, further studies are needed to investigate their translational potential in the real clinical practice.

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Section: Mirna In Atrial Fibrillationmentioning

confidence: 99%

microRNA in Cardiovascular Aging and Age-Related Cardiovascular Diseases

Lucia

Komici²,

Borghetti

et al. 2017

Front. Med.

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“…This binding impairs translation and inhibits the expression of target genes in a small interfering RNA (siRNA)-like manner [1618]. miRNAs are involved in regulating a broad range of biological processes [19][20][21][22][23][24][25], such as signal transduction pathways that are often dysregulated in cancers [2629].…”

mentioning

confidence: 99%

Regulation network and expression profiles of Epstein-Barr virus-encoded microRNAs and their potential target host genes in nasopharyngeal carcinomas

Zeng

Huang

et al. 2014

Sci. China Life Sci.

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Epstein-Barr virus (EBV) is associated with nasopharyngeal carcinoma (NPC) tumorigenesis. However, the mechanism(s) connecting EBV infection and NPC remain unclear. Recently, a new class of EBV microRNAs (miRNAs) has been described. To determine how EBV miRNAs control the expression of host genes, and to understand their potential role in NPC tumorigenesis, we profiled the expression of 44 mature EBV miRNAs and potential host genes in NPC and non-tumor nasopharyngeal epithelial tissues. We found that 40 EBV miRNAs from the BART transcript were highly expressed in NPC. Analysis of potential BART miRNA target genes revealed that 3140 genes and several important pathways might be involved in the carcinogenesis of NPC. A total of 105 genes with potential EBV miRNA binding sites were significantly downregulated, suggesting that EBV miRNAs may regulate these genes and contribute to NPC carcinogenesis. An EBV miRNA and host gene regulation network was generated to provide useful clues for validating of EBV miRNA functions in NPC tumorigenesis.

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“…Moreover, various genetic mutations such as chromosomal loci (10q22-q24 and 6q14-16) mutations, ion channel (Ka + and Na + ) mutations, connexin (GJA5 and GJA1) mutations in the familial AF and more recently several common variants on 4q25, 16q22, and 1q21 in the non-familial AF have been identified (Xiao et al, 2011a,b; Liu et al, 2012a,b). Despite this, the definitive elucidation of AF still remains relatively limited and unclear (Zhang et al, 2011). …”

mentioning

confidence: 99%