4929Contribution of miR-199b to right ventricular remodelling due to pressure overload

Koop, A M C; Duygu, Burcu; Ottaviani, Lara; Poels, Ella; Kolk, K W Van De; Sarvaas, Gideon J. du Marchie; Bartelds, Beatrijs; Lourenço, André P.; Nascimento, Diana S.; Do-O, P Pinto; Falcão-Pires, Inês; Berger, Rolf M. F.; Martins, Paula

doi:10.1093/eurheartj/ehy566.4929

Cited by 2 publications

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“…For example, while in the LV miR-21 exerts a protective role during ventricle remodeling, increased miR-21 levels during RV remodeling correlate with severity of RV hypertrophy [ 201 , 202 ]. In turn, miR-199b is upregulated in both ventricles under pressure overload, but its target genes are differentially affected with DYRKA1 being downregulated in the LV while not being altered in the RV [ 204 , 205 ]. Furthermore, miR-1-5p has been described to be decreased in RV hypertrophy with its target, transforming growth factor beta receptor I ( TGFβR1 ) being upregulated in a MCT rat model.…”

Section: Epigenetic Regulationmentioning

confidence: 99%

Epigenetic Regulation of Pulmonary Arterial Hypertension-Induced Vascular and Right Ventricular Remodeling: New Opportunities?

Kocken

Martins

2020

IJMS

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Pulmonary artery hypertension (PAH) is a rare chronic disease with high impact on patients’ quality of life and currently no available cure. PAH is characterized by constant remodeling of the pulmonary artery by increased proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs), fibroblasts (FBs) and endothelial cells (ECs). This remodeling eventually leads to increased pressure in the right ventricle (RV) and subsequent right ventricle hypertrophy (RVH) which, when left untreated, progresses into right ventricle failure (RVF). PAH can not only originate from heritable mutations, but also develop as a consequence of congenital heart disease, exposure to drugs or toxins, HIV, connective tissue disease or be idiopathic. While much attention was drawn into investigating and developing therapies related to the most well understood signaling pathways in PAH, in the last decade, a shift towards understanding the epigenetic mechanisms driving the disease occurred. In this review, we reflect on the different epigenetic regulatory factors that are associated with the pathology of RV remodeling, and on their relevance towards a better understanding of the disease and subsequently, the development of new and more efficient therapeutic strategies.

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Section: Epigenetic Regulationmentioning

confidence: 99%

Epigenetic Regulation of Pulmonary Arterial Hypertension-Induced Vascular and Right Ventricular Remodeling: New Opportunities?

Kocken

Martins

2020

IJMS

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“…For example, while in the LV miR-21 exerts a protective role during ventricle remodeling, increased miR-21 levels during RV remodeling correlate with severity of RV hypertrophy [201,202]. In turn, miR-199b is upregulated in both ventricles under pressure overload, but its target genes are differentially affected with DYRKA1 being downregulated in the LV while not being altered in the RV [204,205]. Furthermore, miR-1-5p has been described to be decreased in RV hypertrophy with its target, transforming growth factor beta receptor I (TGF-βR1) being upregulated in a MCT rat model.…”

Section: Non-coding Rnas In Right Ventricular Remodelingmentioning

confidence: 99%

Molecular directors

Kocken

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4929Contribution of miR-199b to right ventricular remodelling due to pressure overload

Cited by 2 publications

References 0 publications

Epigenetic Regulation of Pulmonary Arterial Hypertension-Induced Vascular and Right Ventricular Remodeling: New Opportunities?

Epigenetic Regulation of Pulmonary Arterial Hypertension-Induced Vascular and Right Ventricular Remodeling: New Opportunities?

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