Long Non-Coding RNA in Vascular Disease and Aging

Bink, Diewertje I.; Lozano-Vidal, Noelia; Boon, Reinier A.

doi:10.3390/ncrna5010026

Cited by 21 publications

(29 citation statements)

References 118 publications

(152 reference statements)

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“…There is an increasing body of evidence showing that long noncoding RNAs (lncRNAs) and micro RNAs (miRNAs) are involved in cardiovascular aging. LncRNAs act as key regulators of the central aspects of cardiovascular aging (i.e., cardiac hypertrophy, fibrosis, and endothelial/vascular function), and their role in cardiac biology has been recently reviewed [51][52][53][54][55]. A number of miRNAs have been associated with regulation of senescence in various tissues, including the heart [56,57].…”

Section: Cardiac Senescencementioning

confidence: 99%

Regulatory Mechanisms of Mitochondrial Function and Cardiac Aging

Lin

Kerkelä

2020

IJMS

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Aging is a major risk factor for cardiovascular diseases (CVDs), the major cause of death worldwide. Cardiac myocytes, which hold the most abundant mitochondrial population, are terminally differentiated cells with diminished regenerative capacity in the adult. Cardiomyocyte mitochondrial dysfunction is a characteristic feature of the aging heart and one out of the nine features of cellular aging. Aging and cardiac pathologies are also associated with increased senescence in the heart. However, the cause and consequences of cardiac senescence during aging or in cardiac pathologies are mostly unrecognized. Further, despite recent advancement in anti-senescence therapy, the targeted cell type and the effect on cardiac structure and function have been largely overlooked. The unique cellular composition of the heart, and especially the functional properties of cardiomyocytes, need to be considered when designing therapeutics to target cardiac aging. Here we review recent findings regarding key factors regulating cell senescence, mitochondrial health as well as cardiomyocyte rejuvenation.

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Section: Cardiac Senescencementioning

confidence: 99%

Regulatory Mechanisms of Mitochondrial Function and Cardiac Aging

Lin

Kerkelä

2020

IJMS

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“…The mechanistic role of microRNAs (miRNAs, miRs) in cardiovascular pathophysiology is well established. [1][2][3] Substantial evidence has shown that miRNAs can be included in extracellular microvesicles/exosomes, thereby protecting them from ribonuclease-dependent degradation, allowing cell-cell communication. [4][5][6] Cardiac fibroblasts and their activated counterpart (myofibroblasts) have emerged as essential cellular components of normal and postischemic cardiac function.…”

Section: Introductionmentioning

confidence: 99%

Cardiomyocyte‐derived exosomal microRNA‐92a mediates post‐ischemic myofibroblast activation both in vitro and ex vivo

et al. 2020

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Aims We hypothesize that specific microRNAs (miRNAs) within cardiomyocyte‐derived exosomes play a pivotal role in the phenoconversion of cardiac myofibroblasts following myocardial infarction (MI). Methods and results We used an established murine model of MI, obtained in vivo via ligation of the left anterior descending coronary artery. We isolated adult cardiomyocytes and fibroblasts, and we assessed the functional role of cardiomyocyte‐derived exosomes and their molecular cargo in the activation of cardiac fibroblasts. We identified and biologically validated miR‐92a as a transcriptional regulator of mothers against DPP homologues 7 (SMAD7), a known inhibitor of α‐smooth muscle actin (α‐SMA), established marker of myofibroblast activation. We found that miR‐92a was significantly (P < 0.05) upregulated in cardiomyocyte‐derived exosomes and in fibroblasts isolated after MI compared with SHAM conditions (n ≥ 6/group). We tested the activation of myofibroblasts by measuring the expression levels of αSMA, periostin, and collagen. Primary isolated cardiac fibroblasts were activated both when incubated with cardiomyocyte‐derived exosomes isolated from ischemic cardiomyocytes and when cultured in conditioned medium of post‐MI cardiomyocytes, whereas no significant difference was observed following incubation with exosomes or medium from sham cardiomyocytes. These effects were attenuated when an inhibitor of exosome secretion, GW4869 (10 μM for 12 h) was included in the experimental setting. Through means of specific miR‐92a mimic and miR‐92a inhibitor, we also verified the mechanistic contribution of miR‐92a to the activation of cardiac fibroblasts. Conclusions Our results indicate for the first time that miR‐92a is transferred to fibroblasts in form of exosomal cargo and is critical for cardiac myofibroblast activation.

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“…Long noncoding RNA (lncRNA) refers to a class of RNA molecules of more than 200 nucleotides in length which are not translated to proteins. [6][7][8] These special RNA molecules are produced via transcription from intergenic regions of the genome, from within introns of protein-coding genes, or from the antisense strand of a given gene.…”

Section: Introductionmentioning

confidence: 99%

“…Mounting evidence supports the notion that lncRNAs may have important roles in regulating gene expressions, and their functions can be either stimulatory or inhibitory. [6][7][8] The principal molecular mechanisms by which lncRNAs regulate gene expressions include the following: (a) lncRNAs may bind to conventional transcription factors or chromatin-modifying enzymes (such as polycomb 1 repressive complex, histone demethylases, and DNA methyltransferases). 9 This in turn can result in different circumstances.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNAs: Important participants and potential therapeutic targets for myocardial ischaemia reperfusion injury

Ding

Chan

Liu

et al. 2020

Clin Exp Pharma Physio

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Myocardial ischaemia reperfusion (I/R) injury is one of the leading causes of coronary artery disease-associated morbidity and mortality. While different strategies have been used to limit I/R injuries, cardiac functions often do not recover to the normal level as anticipated. Recent studies have pointed to important roles of long noncoding RNAs (lncRNAs) in the development of myocardial I/R injury. LncRNA is a class of RNA molecules of more than 200 nucleotides in length which are not translated into proteins. I/R causes dysregulation of lncRNA expression in cardiomyocytes, thereby How to cite this article: Ding Y-M, Chan EC, Liu L-C, et al. Long noncoding RNAs: Important participants and potential therapeutic targets for myocardial ischaemia reperfusion injury.

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Long Non-Coding RNA in Vascular Disease and Aging

Cited by 21 publications

References 118 publications

Regulatory Mechanisms of Mitochondrial Function and Cardiac Aging

Regulatory Mechanisms of Mitochondrial Function and Cardiac Aging

Cardiomyocyte‐derived exosomal microRNA‐92a mediates post‐ischemic myofibroblast activation both in vitro and ex vivo

Long noncoding RNAs: Important participants and potential therapeutic targets for myocardial ischaemia reperfusion injury

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