Non-coding RNA in endothelial-to-mesenchymal transition

Abstract

Endothelial-to-mesenchymal transition (EndMT) is the process wherein endothelial cells lose their typical endothelial cell markers and functions and adopt a mesenchymal-like phenotype. EndMT is required for development of the cardiac valves, the pulmonary and dorsal aorta, and arterial maturation, but activation of the EndMT programme during adulthood is believed to contribute to several pathologies including organ fibrosis, cardiovascular disease, and cancer. Non-coding RNAs, including microRNAs, long non-coding RNAs, and circular RNAs, modulate EndMT during development and disease. Here, we review the mechanisms by which non-coding RNAs facilitate or inhibit EndMT during development and disease and provide a perspective on the therapeutic application of non-coding RNAs to treat fibroproliferative cardiovascular disease.

Transcriptional regulatory network controlling the ontogeny of hematopoietic stem cells

“…A small group of TF motifs are enriched only in active HE enhancers. Interesting, two of the implicated HE-specific TFs, SNAI1 and TWIST1, are involved in endothelial to mesenchymal transitions (EndMT), a process similar to EHT (Hulshoff et al, 2019).…”

miRNA‐200c‐3p promotes endothelial to mesenchymal transition and neointimal hyperplasia in artery bypass grafts

“…Later studies also support the involvement of this miRNA family in EndoMT [16]. Since controversial and cellular context‐dependent roles for the miR‐200 family in EMT or EndoMT have been widely documented [16,29], more studies are needed to focus on individual members of the miR‐200 family to elucidate their specific role in these pathological conditions. In particular, miR‐200c‐3p has been widely implicated in cardiovascular development and diseases [30].…”

“…Accumulating evidence from preclinical studies and histological observations in humans has provided clear evidence that EndoMT not only plays a fundamental role in normal embryonic developmental processes [14][15][16] but also contributes to a variety of pathological conditions including ventricular diastolic dysfunction [17], atherosclerosis [13,18] and atherosclerotic plaque instability [10], pulmonary arterial hypertension [9], vascular graft remodelling [12], vascular and valvular calcifications [19,20], and tumour progression, among others [15,16,[21][22][23][24]. Therefore, exploring the underlying molecular mechanisms of EndoMT is key to developing novel therapeutic strategies aimed at treating these conditions.…”

“…Therefore, exploring the underlying molecular mechanisms of EndoMT is key to developing novel therapeutic strategies aimed at treating these conditions. Although multiple intercellular mechanisms and signal pathways have been suggested to govern EndoMT [15,16,18,21,22,25,26], the exact molecular mechanisms involved in cardiovascular pathogenesis that occur as a result of EndoMT remain obscure.…”

Genistein alleviates chronic vascular inflammatory response via the miR‑21/NF‑κB p65 axis in lipopolysaccharide‑treated mice

“…Epigenetics is one of the most popular research fields in the post-genomic era, mainly focusing on non-coding RNA, histone modifications, RNA methylation and DNA methylation ( 59 ). miRNAs are non-coding small molecule RNAs ( 60 ). It is considered to be of major clinical importance to discover miRNAs and their target genes in the context of inflammation ( 61 ).…”