Atherosclerosis

Zaina, Silvio; Lund, Gertrud

doi:10.1097/mol.0b013e3283638c47

Cited by 5 publications

(1 citation statement)

References 9 publications

(6 reference statements)

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“…The abnormal DNA methylation is another common abnormality during the development of atherosclerosis. Some studies showed that the significant global DNA hypomethylation is considered one of the landmarks of advanced atherosclerosis and this abnormality affected the expression of many genes resulting in dysfunctions of a variety of cells (such as VEC, VSMC and immune cells) [8] . However, in spite of the hypomethylation of genomic DNA, the hypermethylation of many genes was also found.…”

Section: Introductionmentioning

confidence: 99%

Integrated Analysis of Microarray Data of Atherosclerotic Plaques: Modulation of the Ubiquitin-Proteasome System

et al. 2014

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Atherosclerosis is a typical complex multi-factorial disease and many molecules at different levels and pathways were involved in its development. Some studies have investigated the dysregulation in atherosclerosis at mRNA, miRNA or DNA methylation level, respectively. However, to our knowledge, the studies that integrated these data and revealed the abnormal networks of atherosclerosis have not been reported. Using microarray technology, we analyzed the omics data in atherosclerosis at mRNA, miRNA and DNA methylation levels. Our results demonstrated that the global DNA methylation and expression of miRNA/mRNA were significantly decreased in atherosclerotic plaque than in normal vascular tissue. The interaction network constructed using the integrative data revealed many genes, cellular processes and signaling pathways which were widely considered to play crucial roles in atherosclerosis and also revealed some genes, miRNAs or signaling pathways which have not been investigated in atherosclerosis until now (e.g. miR-519d and SNTB2). Moreover, the overall protein ubiquitination in atherosclerotic plaque was significantly increased. The proteasome activity was increased early but decreased in advanced atherosclerosis. Our study revealed many classic and novel genes and miRNAs involved in atherosclerosis and indicated the effects of ubiquitin-proteasome system on atherosclerosis might be closely related to the course of atherosclerosis. However, the efficacy of proteasome inhibitors in the treatment of atherosclerosis still needs more research.

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Section: Introductionmentioning

confidence: 99%

Integrated Analysis of Microarray Data of Atherosclerotic Plaques: Modulation of the Ubiquitin-Proteasome System

et al. 2014

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Epigenetics of the failing heart

Marı́n-Garcı́a

Akhmedov

2015

Heart Fail Rev

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With the impressive advancement in high-throughput 'omics' technologies over the past two decades, epigenetic mechanisms have emerged as the regulatory interface between the genome and environmental factors. These mechanisms include DNA methylation, histone modifications, ATP-dependent chromatin remodeling and RNA-based mechanisms. Their highly interdependent and coordinated action modulates the chromatin structure controlling access of the transcription machinery and thereby regulating expression of target genes. Given the rather limited proliferative capability of human cardiomyocytes, epigenetic regulation appears to play a particularly important role in the myocardium. The highly dynamic nature of the epigenome allows the heart to adapt to environmental challenges and to respond quickly and properly to cardiac stress. It is now becoming evident that histone-modifying and chromatin-remodeling enzymes as well as numerous non-coding RNAs play critical roles in cardiac development and function, while their dysregulation contributes to the onset and development of pathological cardiac remodeling culminating in HF. This review focuses on up-to-date knowledge about the epigenetic mechanisms and highlights their emerging role in the healthy and failing heart. Uncovering the determinants of epigenetic regulation holds great promise to accelerate the development of successful new diagnostic and therapeutic strategies in human cardiac disease.

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