Noncoding RNA in age-related cardiovascular diseases

Simona Greco, Myriam Gorospe, Fabio Martelli, Simona Greco, Myriam Gorospe, Fabio Martelli

Abstract

Eukaryotic gene expression is tightly regulated transcriptionally and post-transcriptionally by a host of noncoding (nc)RNAs. The best-studied class of short ncRNAs, microRNAs, mainly repress gene expression post-transcriptionally. Long noncoding (lnc)RNAs, which comprise RNAs differing widely in length and function, can regulate gene transcription as well as post-transcriptional mRNA fate. Collectively, ncRNAs affect a broad range of age-related physiologic deteriorations and pathologies, including reduced cardiovascular vigor and age-associated cardiovascular disease. This review presents an update of our understanding of regulatory ncRNAs contributing to cardiovascular health and disease as a function of advancing age. We will discuss (1) regulatory ncRNAs that control aging-associated cardiovascular homeostasis and disease, (2) the concepts, approaches, and methodologies needed to study regulatory ncRNAs in cardiovascular aging and (3) the challenges and opportunities that age-associated regulatory ncRNAs present in cardiovascular physiology and pathology. This article is part of a Special Issue entitled "CV Aging".

Keywords: Aging; Cardiovascular disease; Long noncoding RNA; MicroRNA.

Copyright © 2015 Elsevier Ltd. All rights reserved.

Figures

Fig. 1
Fig. 1
Senescence-associated ncRNAs. Several studies have identified ncRNAs upregulated and downregulated in senescence, but only few have been shown to modulate senescence experimentally. The figure shows microRNAs (blue) and lncRNAs (green) directly implicated in molecular pathways that govern cell senescence.
Fig. 2
Fig. 2
miR-200 regulates endothelial dysfunction and cardiovascular complications linked to diabetes and obesity. ROS production or pathologies associated to elevated ROS production play a causal role in endothelial and cardiovascular diseases. (Left) MiR-200c and miR-141 are among the most highly upregulated miRNAs in diabetic mouse heart; accordingly, the target of miR-200 SLC25A3, a protein essential for ATP production, declines in type 1 diabetes, reducing ATP production and cell viability. (Center) In Zucker obese rats, a genetic model for obesity, hypertension and cardiac dysfunction, elevated miR-200c activates a compensatory mechanism to down-regulate excessive activation of the nutrient sensor kinase S6K1, involved in adipocyte lineage commitment. (Right) MiR-200c levels rise following oxidative stress; the ensuing inhibition of its target ZEB1 induces cell growth arrest, apoptosis and cellular senescence.
Fig. 3
Fig. 3
miR-210 regulates mitochondrial activity. miR-210 represses target ISCU1, ISCU2, COX10 and FECH mRNAs, encoding proteins that directly or indirectly affect the mitochondrial respiratory chain and reduce ROS production.
Fig. 4
Fig. 4
miR-216a regulates autophagy. miR-216a activity on its targets BECN1 and ATG5 inhibits autophagy and stimulates ox-LDL accumulation in EC as well as monocyte adhesion and migration.
Fig. 5
Fig. 5
SIRT1 regulation by miRNAs in ECs. miR-217 downregulates SIRT1 expression. This leads to lower deacetylation of its targets FOXO1 and eNOS, rendering them inactive and triggering senescence (left). By targeting SIRT1 expression, miR-132 decreases SREBP-1c acetylation and increases its activity, promoting the accumulation of fatty acids and cholesterol (center). In TGF-β-treated ECs, miR-212 reduces SIRT1 abundance, inhibits endothelial migration and capillary tube formation, and stimulates Notch signaling via NRARP (right).
Fig. 6
Fig. 6
SIRT1 regulation by miRNAs in cardiomyocytes. In cardiomyocytes, the free fatty acid palmitate increases miR-195 levels, which in turn inhibits SIRT1 and promotes ROS-triggered apoptosis (left). In hypoxic cardiomyocytes, downregulation of miR-199a increases HIF-1α levels and p53-mediated cardiomyocyte apoptosis (center). In normoxic cardiomyocytes, low miR-199a raises SIRT1 and HIF-1α levels, simulating preconditioning (right).

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