Abstract
If we consider the molecular size of major nucleic acids and the time elapsed since we knew about their existence, microRNAs (miRs) comparatively appear as recently discovered and structurally small pieces of genetic material, but we should make no mistake to underestimate these modest but powerful molecules. Regulating no less than half of the transcriptome, their influence is a key for the fine-tuning of almost any biological process. miRs are considered elements that add precision and robustness to a myriad of physiological and pathological processes and commonly function as components of cellular networks by buffering extremes in gene expression. Their small size limits the side effects of these molecules and eases a pervasive behavior that explains their presence in different body fluids but also opens a complete new field of clinical opportunities for diagnostic, prognostic, or risk stratification applications which benefit from the possibility of bedside measurement.
From a purely investigational perspective, miRs constitute also a very useful tool. Their pleiotropic repressing effect on various, often functionally related, target mRNAs gives us clues on the molecular mechanisms underlying many pathological phenomena. On the other hand, since mRNA complementarity is dictated by a relatively short sequence (seed region) of nucleotides in the miR, computer-based prediction of miR targets is readily available. Additionally, “the control on the controllers” is tempting with the aim of modifying favorably the natural history of miR-related diseases. Several techniques to block or overexpress miRs have been launched, and, even though there are significant difficulties and drawbacks in their administration, some of them are starting to be used in human therapeutics.
miR-133 is muscle specific and one of the most abundant miRs in the heart. It plays major roles in the developing heart on cell differentiation into muscle tissue and also in later stages of cardiac morphogenesis. It is included among the handful of molecules able to cooperate for the experimental reprogrammation of fibroblasts into cardiac-like myocytes. miR-133 participates in the molecular pathology of myocardial hypertrophy, be it primary or secondary, in the transition and evolution of cardiac failure, in myocardial fibrosis and in cardiac cell apoptosis. In stable coronary artery disease and, particularly, in the acute coronary events, miR-133 levels decrease in the myocardium and increase in the circulation proportionally to the extent of the infarcted area. The value of circulating levels of miR-133 as a diagnostic and prognostic biomarker in these patients during the acute ischemic episode and after primary revascularization has already been established. Finally, research studies undertaken during the last 5 years show that dysregulation of miR-133 contributes to the pathological vascular remodeling underlying essential hypertension, vascular calcification, atherosclerosis, and aneurysmal disease.
At this time, it could be said that miRs are ready for prime time for diagnostic and prognostic purposes in the clinical arena, but more is coming on miR molecular manipulation with miR mimics and anti-miRs and even more with targeting of miR-related pathways. Meanwhile, other future uses of miRs in the fields of regenerative medicine and tissue engineering await for further refinement before they can be clinically applicable.
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Abbreviations
- AAA:
-
Abdominal aortic aneurysm
- ACS:
-
Acute coronary syndrome
- AMI:
-
Acute myocardial infarction
- BAV:
-
Bicuspid aortic valve
- ceRNA:
-
Competing endogenous RNA
- CHD:
-
Coronary heart disease
- CTGF:
-
Connective tissue growth factor
- cTn:
-
Cardiac troponin
- ICA:
-
Intracranial aneurysm
- lnc-RNA:
-
Long noncoding RNA
- LV:
-
Left ventricle
- LVAD:
-
Left ventricular assist device
- MI:
-
Myocardial infarction
- miR:
-
MicroRNA
- MMP:
-
Matrix metalloproteinase
- MRE:
-
miR recognition element
- NSTEMI:
-
Non ST-elevation myocardial infarction
- qRT-PCR:
-
Real-time polymerase chain reaction
- ROC:
-
Receiver operating characteristic
- STEMI:
-
ST-elevation myocardial infarction
- TAA:
-
Thoracic aortic aneurysm
- TAC:
-
Transverse aortic constriction
- TAD:
-
Thoracic aortic dissection
- TAV:
-
Tricuspid aortic valve
- TGF-β:
-
Transforming growth factor-β
- UA:
-
Unstable angina
- UTR:
-
Untranslated region
- VSMC:
-
Vascular smooth muscle cell
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Acknowledgments
This work was supported by the Ministerio de Economía y Competitividad, Spanish Government [Instituto de Salud Carlos III (PI12/00999 and RETICS RD12/0042/0018); SAF2013-47434-Retos].
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Definitions
- Anti-miRs
-
Synthetic single-stranded antisense oligonucleotides that hybridize by base pairing to target miRs and block their function.
- Cardiac remodeling
-
Genome expression resulting in molecular, cellular, and interstitial changes and manifested clinically as changes in size, shape, and function of the heart originated from cardiac load or injury.
- MicroRNAs (miRs)
-
Short non-coding, single-stranded RNAs involved in the posttranscriptional control of gene expression. miR binding to its mRNA targets results in the inhibition of translation to proteins.
- miR-133
-
Muscle-specific miR that is expressed by skeletal and cardiac striated myocytes and by smooth muscle cells.
- miR cluster
-
miRs transcribed as a single unit from the same primary transcript that are regulated in a similar way.
- miR family
-
Group of miRs that have identical seed regions and share targets and functions. The occurrence of miRs belonging to distinct “seed” families within the same cluster is common.
- miR recognition element (MRE)
-
mRNA sequence in the 3′-UTR end that binds a specific miR usually by partial or complete base pairing.
- miR sponges
-
Are synthetic RNA molecules harboring complementary binding sites to the seed sequences of a given miR or a miR family.
- Myomirs
-
Group of miRs that are highly expressed in muscular tissue.
- Seed region
-
Sequence of 6–8 nucleotides at the 5′ end of miRs which binds by base pairing with complementary sequences of target mRNAs.
- Transverse aortic constriction
-
Experimental model of LV pressure overload induced by surgical banding of the mid aortic arch.
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Nistal, J.F., Villar, A.V., García, R., Hurlé, M.A. (2015). MicroRNA-133: Biomarker and Mediator of Cardiovascular Diseases. In: Patel, V., Preedy, V. (eds) Biomarkers in Cardiovascular Disease. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-7741-5_28-1
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