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J Am Coll Cardiol. 2014 Mar 11;63(9):920-7. doi: 10.1016/j.jacc.2013.09.041. Epub 2013 Oct 23.

Circulating miR-29a, among other up-regulated microRNAs, is the only biomarker for both hypertrophy and fibrosis in patients with hypertrophic cardiomyopathy.

Author information

1
Institute of Genetics and Biomedical Research, Milan Unit, Milan, Italy; Multimedica Research Hospital, Milan, Italy.
2
Multimedica Research Hospital, Milan, Italy.
3
Department of Advanced Biomedical Sciences, Federico II University, Naples, Italy.
4
Department of Medical-Surgical Sciences and Biotechnology, La Sapienza University of Rome, Rome, Italy.
5
Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands.
6
Department of Biomedical, Biotechnological and Translational Sciences, University of Parma, Parma, Italy.
7
AVIS Comunale Milano, Milan, Italy.
8
Humanitas Clinical and Research Center and University of Milan, Rozzano, Italy.
9
Department of Advanced Biomedical Sciences, Federico II University, Naples, Italy. Electronic address: sandro.betocchi@unina.it.
10
Institute of Genetics and Biomedical Research, Milan Unit, Milan, Italy; Humanitas Clinical and Research Center and University of Milan, Rozzano, Italy. Electronic address: gianluigi.condorelli@unimi.it.

Abstract

OBJECTIVES:

The purpose of this paper was to determine whether microRNAs (miRNAs) involved in myocardial remodeling were differentially expressed in the blood of hypertrophic cardiomyopathy (HCM) patients, and whether circulating miRNAs correlated with the degree of left ventricular hypertrophy and fibrosis.

BACKGROUND:

miRNAs-small, noncoding ribonucleic acids (RNAs) that regulate gene expression by inhibiting RNA translation-modulate cellular function. Myocardial miRNAs modulate processes such as cardiomyocyte (CM) hypertrophy, excitation-contraction coupling, and apoptosis; non-CM-specific miRNAs regulate myocardial vascularization and fibrosis. Recently, the possibility that circulating miRNAs may be biomarkers of cardiovascular disease has been raised.

METHODS:

Forty-one HCM patients were characterized with conventional transthoracic echocardiography and cardiac magnetic resonance. Peripheral plasma levels of 21 miRNAs were assessed by quantitative real-time polymerase chain reaction and were compared with levels in a control group of 41 age- and sex-matched blood donors.

RESULTS:

Twelve miRNAs (miR-27a, -199a-5p, -26a, -145, -133a, -143, -199a-3p, -126-3p, -29a, -155, -30a, and -21) were significantly increased in HCM plasma. However, only 3 miRNAs (miR-199a-5p, -27a, and -29a) correlated with hypertrophy; more importantly, only miR-29a correlated also with fibrosis.

CONCLUSIONS:

Our data suggest that cardiac remodeling associated with HCM determines a significant release of miRNAs into the bloodstream: the circulating levels of both cardiac- and non-cardiac-specific miRNAs are significantly increased in the plasma of HCM patients. However, correlation with left ventricular hypertrophy parameters holds true for only a few miRNAs (i.e., miR-199a-5p, -27a, and -29a), whereas only miR-29a is significantly associated with both hypertrophy and fibrosis, identifying it as a potential biomarker for myocardial remodeling assessment in HCM.

KEYWORDS:

circulating microRNAs; fibrosis; hypertrophic cardiomyopathy; myocardial remodeling

PMID:
24161319
DOI:
10.1016/j.jacc.2013.09.041
[Indexed for MEDLINE]
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