MicroRNA-142-3p improves vascular relaxation in uremia

Kétszeri, Máté; Kirsch, Andrijana; Frauscher, Bianca; Moschovaki-Filippidou, Foteini; Mooslechner, Agnes A.; Kirsch, Alexander H.; Schabhuettl, Corinna; Aringer, Ida; Artinger, Katharina; Pregartner, Gudrun; Ekart, Robert; Breznik, Silva; Hojs, Radovan; Goessler, Walter; Schilcher, Irene; Müller, H.; Obermayer–Pietsch, Barbara; Frank, Saša; Rosenkranz, Alexander R.; Eller, Philipp; Eller, Kathrin

doi:10.1016/j.atherosclerosis.2018.11.024

Cited by 20 publications

(15 citation statements)

References 27 publications

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“…Moreover, we further identified 8 miRNAs that were upregulated, including miR-17-1-3p, miR-142-5p, miR-142-3p, miR-151-5p, miR-215, miR-539-5p, miR-1247-5p and miR-1298. These findings were consistent with those reported in previous studies [19][20][21][22][23][24], which revealed that these miRNAs play important roles in vascular function. GO and KEGG-pathway enrichment analysis of predicted target genes further confirmed that these differentially expressed miRNAs are involved in the immunological inflammatory reactions and metabolisms.…”

Section: Discussionsupporting

confidence: 93%

Comparative analysis of relative gene expression data reveals novel microRNAs in the artery of rats with renovascular hypertension

Wang

2020

ARCH BIOL SCI BELGRA

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Hypertension is associated with impaired vascular endothelial function. However, the regulatory mechanisms of vascular dysfunction in rats with renovascular hypertension (RVH) remain poorly understood. In this study, the 2-kidney-1-clip (2K1C) hypertensive rat model was utilized. Next-generation sequencing was then used to detect microRNA (miRNA) expression profiling in the arteries of 2K1C rats. We identified 17 miRNAs that were differentially expressed in the 2K1C group compared with the sham group, of which 9 were downregulated and 8 were upregulated. These differentially expressed miRNAs were found to be associated with immune/inflammatory and metabolic pathways, which are involved in vascular dysfunction. Treatment with losartan maintained the expression of the differentially expressed miRNAs, miR-31a-5p and miR-142-3p, and the levels of TNF-?, IL-1?, IL-6 and MCP-1, indicating that the differentially expressed miRNAs and their associated immune/inflammatory pathways play a pivotal role in the modulation of the vascular dysfunction in 2K1C rats. Our study provides valuable information about miRNA expression in the arteries of 2K1C rats, expanding our understanding of the complex molecular mechanisms underlying the vascular dysfunction in rats with RVH.

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Section: Discussionsupporting

confidence: 93%

Comparative analysis of relative gene expression data reveals novel microRNAs in the artery of rats with renovascular hypertension

Wang

2020

ARCH BIOL SCI BELGRA

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“…A drug of this class, vericiguat, reduced death from CV causes or hospitalization for heart failure in a large trial in patients with heart failure [226]. Finally, both in uremic animals and humans, microRNAs have emerged as significant mediators of uremia-induced ED [227][228][229], thereby constituting a potential therapeutic target to ameliorate endothelial injury and arterial disease in CKD.…”

Section: Novel Therapeutic Approachesmentioning

confidence: 99%

Endothelial Dysfunction in Chronic Kidney Disease, from Biology to Clinical Outcomes: A 2020 Update

Roumeliotis

Mallamaci

Zoccali

2020

JCM

132

128

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The vascular endothelium is a dynamic, functionally complex organ, modulating multiple biological processes, including vascular tone and permeability, inflammatory responses, thrombosis, and angiogenesis. Endothelial dysfunction is a threat to the integrity of the vascular system, and it is pivotal in the pathogenesis of atherosclerosis and cardiovascular disease. Reduced nitric oxide (NO) bioavailability is a hallmark of chronic kidney disease (CKD), with this disturbance being almost universal in patients who reach the most advanced phase of CKD, end-stage kidney disease (ESKD). Low NO bioavailability in CKD depends on several mechanisms affecting the expression and the activity of endothelial NO synthase (eNOS). Accumulation of endogenous inhibitors of eNOS, inflammation and oxidative stress, advanced glycosylation products (AGEs), bone mineral balance disorders encompassing hyperphosphatemia, high levels of the phosphaturic hormone fibroblast growth factor 23 (FGF23), and low levels of the active form of vitamin D (1,25 vitamin D) and the anti-ageing vasculoprotective factor Klotho all impinge upon NO bioavailability and are critical to endothelial dysfunction in CKD. Wide-ranging multivariate interventions are needed to counter endothelial dysfunction in CKD, an alteration triggering arterial disease and cardiovascular complications in this high-risk population.

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“…One such target investigated is miR-142-3p which is inversely correlated with carotid-femoral pulse wave velocity in humans as an indicator of vascular stiffness and is significantly decreased in patients with ESRD [172]. Also, in uremic mice with markedly reduced acetylcholine-induced relaxation, intravenous injection of synthetic mimic syn-mmu-mir-142-3p in order to restore bioavailability of miR-142-3p 2 days before sacrifice increased aortic relaxation of aortic rings to control levels [172].…”

Section: Extracellular Vesicles As Intercellular Messengers In Ckd and Cadmentioning

confidence: 99%

Vascular pathologies in chronic kidney disease: pathophysiological mechanisms and novel therapeutic approaches

et al. 2021

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Cardiovascular disease (CVD) is a major cause of death in patients with chronic kidney disease (CKD). Both conditions are rising in incidence as well as prevalence, creating poor outcomes for patients and high healthcare costs. Recent data suggests CKD to be an independent risk factor for CVD. Accumulation of uremic toxins, chronic inflammation, and oxidative stress have been identified to act as CKD-specific alterations that increase cardiovascular risk. The association between CKD and cardiovascular mortality is markedly influenced through vascular alterations, in particular atherosclerosis and vascular calcification (VC). While numerous risk factors promote atherosclerosis by inducing endothelial dysfunction and its progress to vascular structural damage, CKD affects the medial layer of blood vessels primarily through VC. Ongoing research has identified VC to be a multifactorial, cell-mediated process in which numerous abnormalities like mineral dysregulation and especially hyperphosphatemia induce a phenotype switch of vascular smooth muscle cells to osteoblast-like cells. A combination of pro-calcifying stimuli and an impairment of inhibiting mechanisms like fetuin A and vitamin K-dependent proteins like matrix Gla protein and Gla-rich protein leads to mineralization of the extracellular matrix. In view of recent studies, intercellular communication pathways via extracellular vesicles and microRNAs represent key mechanisms in VC and thereby a promising field to a deeper understanding of the involved pathomechanisms. In this review, we provide an overview about pathophysiological mechanisms connecting CKD and CVD. Special emphasis is laid on vascular alterations and more recently discovered molecular pathways which present possible new therapeutic targets.

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MicroRNA-142-3p improves vascular relaxation in uremia

Cited by 20 publications

References 27 publications

Comparative analysis of relative gene expression data reveals novel microRNAs in the artery of rats with renovascular hypertension

Comparative analysis of relative gene expression data reveals novel microRNAs in the artery of rats with renovascular hypertension

Endothelial Dysfunction in Chronic Kidney Disease, from Biology to Clinical Outcomes: A 2020 Update

Vascular pathologies in chronic kidney disease: pathophysiological mechanisms and novel therapeutic approaches

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