Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Editorial
. 2009 Jan 30;104(2):138-40.
doi: 10.1161/CIRCRESAHA.108.192492.

Searching for miR-acles in cardiac fibrosis

Eva van Rooij, Eric N Olson
Editorial

Searching for miR-acles in cardiac fibrosis

Eva van Rooij et al. Circ Res. .
No abstract available

PubMed Disclaimer

Conflict of interest statement

Disclosures: The authors are cofounders of miRagen Therapeutics, a company based on the therapeutic application of miRNAs in heart disease.

Figures

Figure 1
Figure 1. miRNAs involved in cardiac fibrosis
A histological section of a hypertrophic heart is shown. Hypertrophic cardiomyocytes are surrounded by excessive extracellular matrix (shown in blue). miRNAs implicated in cardiac fibrosis are indicated.
Figure 2
Figure 2. Mechanism for miRNA-mediated fibrosis in response to cardiac stress
Cardiac fibrosis is the result of both an increase in fibroblast proliferation and an extracellular matrix deposition. Stress leads to up-regulation of miR-21 and down-regulation of miR-29 and miR-30 in cardiac fibroblasts, as well as down-regulation of miR-30 and miR-133 in cardiomyocytes. miR-21 represses Sprouty homolog 1 (Spry1), a negative regulator of ERK-MAP kinase signaling, thereby leading to fibroblast proliferation and fibrosis. miR-29 represses expression of collagens, and miR-30 and -133 repress expression of CTGF, a positive regulator of fibrosis. TGF-β also promotes fibrosis by repressing expression of miR-29, -30 and -133.
See this image and copyright information in PMC

Comment on

References

    1. Duisters RF, Tijsen AJ, Schroen B, Leenders JJ, Lentink V, van der Made I, Herias V, van Leeuwen RE, Schellings MW, Barenbrug P, Maessen JG, Heymans S, Pinto YM, Creemers EE. miR-133 and miR-30 Regulate Connective Tissue Growth Factor. Implications for a Role of MicroRNAs in Myocardial Matrix Remodeling. Circ Res. 2009;104:XXX–XXX. - PubMed
    1. Hill JA, Olson EN. Cardiac plasticity. N Engl J Med. 2008;358(13):1370–1380. - PubMed
    1. Khan R, Sheppard R. Fibrosis in heart disease: understanding the role of transforming growth factor-beta in cardiomyopathy, valvular disease and arrhythmia. Immunology. 2006;118(1):10–24. - PMC - PubMed
    1. Ouzounian M, Lee DS, Liu PP. Diastolic heart failure: mechanisms and controversies. Nat Clin Pract Cardiovasc Med. 2008;5(7):375–386. - PubMed
    1. Daniels A, van Bilsen M, Goldschmeding R, van der Vusse GJ, van Nieuwenhoven FA. Connective tissue growth factor and cardiac fibrosis. Acta Physiol (Oxf) 2008 - PubMed

MeSH terms