Long Noncoding RNAs and MicroRNAs in Cardiovascular Pathophysiology

Thum, Thomas; Condorelli, Gianluigi

doi:10.1161/circresaha.116.303549

Cited by 341 publications

(260 citation statements)

References 140 publications

(141 reference statements)

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“…Recently, micro RNAs (miRNAs) have attracted much attention due to their important roles in almost all biological processes, [8][9][10][11] and have emerged as promising candidates as therapeutics for a wide variety of diseases. 12,13) In this issue, Jing and colleagues have provided evidence that miR-99a attenuates lipopolysaccharide (LPS)-induced oxidative injury in rat cardiomyocyte H9c2 cells.…”

Section: Article P422mentioning

confidence: 99%

“…This association yields mRNA repression either by transcript destabilization, translational inhibition, or both. [8][9][10][11]15) LPS is a critical substance responsible for myocardial dysfunction in sepsis, and stimulation with LPS induces cardiomyocyte injury through multiple mechanisms including enhanced oxidative stress. 16,17) Jing and colleagues demonstrated that transfecting H9c2 cells with miR-99a mimic prevented LPS-induced apoptotic cell death, which was associated with a decrease in ROS generation.…”

Section: Article P422mentioning

confidence: 99%

“…31) Further studies are necessary to determine whether overexpression of miR-99a also attenuates LPS-induced myocardial oxidative injury and dysfunction without altering physiological ROS signaling in a A number of miRNAs have been identified that are expressed in cardiac tissue and thus likely to play a key role in cardiac physiology and pathophysiology. 8,10,11,15) These include miR-1, miR-21, miR-22, miR-23a, miR-25, miR-133, miR-145, miR-199a, miR-208, miR-214, miR-378, miR-494, and miR-574-3p. For example, miR-21 mediated anti-apoptotic effects of Akt by direct suppression of mRNA expression of Fas ligand (Fasl), and transgenic overexpression of miR-21 reduced infarct size in a murine model of ischemia/reperfusion.…”

Section: Article P422mentioning

confidence: 99%

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MicroRNA-99a

Liu

Akazawa

2017

Int. Heart J.

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R eactive oxygen species (ROS) are continuously formed in myocardium as a byproduct of mitochondrial oxidative phosphorylation, and are also produced by several enzymes such as NADPH oxidases, xanthine oxidase, and uncoupled endothelial NO synthase.1,2) In normal cardiovascular physiology, ROS act as essential signaling molecules that modulate the activity of many bioactive molecules including protein kinases, phosphatases, transcription factors, and cytoskeletal proteins.3) However, excessive and aberrant production of ROS during pathological oxidative stress can cause cellular dysfunction and death by inducing irreversible damage of organelles and macromolecules such as lipids, proteins, and DNA.1,2) An increasing body of evidence has suggested that oxidative stress is crucially involved in the pathogenesis and progression of a wide range of cardiovascular diseases.1,2) For example, it was reported that the myocardial ROS levels were elevated in animal models of ischemia-reperfusion injury 2,4) and heart failure, 5) and that a number of antioxidant strategies using ROS scavengers provided cardioprotection in these animal models.2) However, clinical interventions by treatment with antioxidants have proven to be ineffective or even harmful for patients with cardiovascular diseases.2,6) Rather than simple antioxidant strategies, a strategy to reduce pathological oxidative stress without altering physiological ROS signaling will put forward the translation of ROS modulation into the clinic. 7)

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Section: Article P422mentioning

confidence: 99%

Section: Article P422mentioning

confidence: 99%

Section: Article P422mentioning

confidence: 99%

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MicroRNA-99a

Liu

Akazawa

2017

Int. Heart J.

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“…LncRNA are, in general, expressed at relatively low levels and are far less well conserved than miRNA [56][57][58]. LncRNA can be classified into different subtypes based on their genomic location: sense lncRNAs, antisense lncRNAs, bidirectional lncRNAs, intronic lncRNAs and intergenic lncRNAs [59]. LncRNAs have diverse molecular mechanisms of regulating gene expression through interactions with DNA, RNA, or protein, by acting as decoys, scaffolds, guides or signalling molecules (Figure 1).…”

Section: Lncrna Transcription and Functionmentioning

confidence: 99%

Role of noncoding RNA in vascular remodelling

Lin

Bradshaw

Baker

2016

Current Opinion in Lipidology

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Purpose of review: Non-coding RNA (ncRNAs), such as microRNAs (miRNAs) and long non-coding RNAs (LncRNAs), are becoming fundamentally important in the pathophysiology relating to injury-induced vascular remodelling. We highlight recent studies that demonstrate the involvement of ncRNAs in vein graft disease, in in-stent restenosis (ISR) and in pulmonary arterial hypertension (PAH), with a particular focus on endothelial cell (EC) and vascular smooth muscle cell (VSMC) function. We also briefly discuss the emerging role of exosomal-derived ncRNAs and how this mechanism impacts on vascular function.

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“…[14] The posttranslational regulatory roles of microRNAs have been shown in almost all physiological processes via non-precise complementary binding to the 3'un-translated region of target mRNA, which results in translation repression or mRNA degradation. [14] Taking advantage of the remarkable stability of microRNAs in serum and body fluids [15] and the dysregulated expression of microRNAs under disease conditions, [16] many studies have proposed microRNAs as diagnostic and prognostic biomarkers. [17,18] Recently, a few prospective studies have revealed the altered expression of microRNAs in heart tissue/ plasma of patients with CHD versus CHD-free controls (Table 1).…”

Section: Introductionmentioning

confidence: 99%