Potential roles of microRNA-1 and microRNA-133 in cardiovascular disease

Reviews in Cardiovascular Medicine  2020, Vol. 21 Issue (1): 57-64     DOI: 10.31083/j.rcm.2020.01.577 Potential roles of microRNA-1 and microRNA-133 in cardiovascular disease Zhipeng Song1, Rui Gao2, Bo Yan3, 4, 5, *() 1 Department of Medicine, Shandong University School of Medicine, Jinan, Shandong, 250014, P. R. China
2 Cardiovascular Medicine Department, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, 272000, P. R. China
3 Shandong Provincial Key Laboratory of Cardiac Disease Diagnosis and Treatment, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, 272000,
P. R. China
4 Shandong Provincial Sino-US Cooperation Research Center for Translational Medicine, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, 272000, P. R. China
5 The Center for Molecular Genetics of Cardiovascular Diseases, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, 272000, P. R. China Abstract:

Cardiovascular disease is still the main cause of morbidity and mortality worldwide. Currently, the frontier of research into cardiovascular disease is the field of non-coding RNA. In this review, information was collected on the use of micro-RNAs as non-invasive biomarkers and their role in pathophysiological processes and therapeutic applications. In the case of microRNA-1 and microRNA-133, the roles and regulatory mechanisms of them are reviewed for arrhythmia, myocardial infarction, diabetic cardiomyopathy, myocardial hypertrophy, cardiomyocyte differentiation, and cell reprogramming. It was observed that microRNA-1 and microRNA-133 do not exist independently, but are two co-transcriptional and cooperative regulatory factors. They have diagnostic value as biomarkers, but also have the potential as therapeutic targets such as for antiarrhythmia and cardiac reprogramming.

Submitted:  15 October 2019      Accepted:  14 February 2020      Published:  30 March 2020      Fund: 
81870279/National Natural Science Foundation of China *Corresponding Author(s):  Bo Yan     E-mail:  yanbo@mail.jnmc.edu.cn Service E-mail this article Add to citation manager E-mail Alert RSS Articles by authors Zhipeng Song    Rui Gao    Bo Yan   

Figure 1.  Model of miR-1 and miR-133-mediated regulation of arrhythmia. MiR-1 and miR-133 co-regulate arrhythmia. The red dotted line indicates the regulation that needs to be verified. AA, arachidonic acid; CYP450, Cytochrome P450; EETs, epoxyeicosatrienoic acids; sEH, soluble epoxide hydrolase; sEHi, soluble epoxide hydrolase inhibitor; DHETs, dihydroxyeicosatrienoic acids; miR-133, microRNA-133; KCNQ1, potassium voltage-gated channel subfamily Q member 1; IKs, slow delayed rectifier K+ current; KCNH2, potassium voltage-gated channel subfamily H member 2; ERG, ether-a-go-go related gene; IKr, delayed rectifier K+ current; miR-1, microRNA-1; KCNJ2, potassium voltage-gated channel subfamily J member 2; Kir2.1, inwardly rectifying K channel 2.1; GJA1, gap junction protein alpha 1; Cx43, connexin 43.


Figure 2.  Model of miR-1 and miR-133-mediated regulation of myocardial hypertrophy and cell differentiation. MiR-1 and miR-133 regulate myocardial hypertrophy and cell differentiation synergistically. The black dotted line indicates indirect regulation, and the red dotted line indicates the regulation that needs to be verified. miR-133, microRNA-133; SRF, serum response factor; CArG, [CC (A/T) 6GG]; GATA4, GATA binding protein 4; miR-1, microRNA-1; Ca, Calcium; CaM, calcium-binding protein calmodulin; CN, calcineurin; NFAT, nuclear factor of the activated T cell; CaMK, calcium-calmodulin dependent protein kinase; MEF2a, myocyte enhancer factor 2a; HDAC4, histone deacetylase 4; MEF2, myocyte enhancer factor 2; MyoD, myogenic determination factor.


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