The DOI matches its Crossref record; 81 of the 81 references it cites were found in a registry or an index.
Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart
Abstract
When considering the pathological steps in the progression from cardiac overload towards the full clinical syndrome of heart failure, it is becoming increasingly clear that the extracellular matrix (ECM) is an important determinant in this process. Chronic pressure overload induces a number of structural alterations, not only hypertrophy of cardiomyocytes but also an increase in ECM proteins in the interstitium and perivascular regions of the myocardium. When this culminates in excessive fibrosis, myocardial compliance decreases and electrical conduction is affected. Altogether, fibrosis is associated with an increased risk of ventricular dysfunction and arrhythmias. Consequently, anti-fibrotic strategies are increasingly recognized as a promising approach in the prevention and treatment of heart failure. Thus, dissecting the molecular mechanisms underlying the development of cardiac fibrosis is of great scientific and therapeutic interest. In this review, we provide an overview of the available evidence supporting the general idea that fibrosis plays a causal role in deteriorating cardiac function. Next, we will delineate the signalling pathways importantly governed by transforming growth factor β (TGFβ) in the control of cardiac fibrosis. Finally, we will discuss the recent discovery that miRNAs importantly regulate cardiac fibrosis.
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Cites
The Effect of Spironolactone on Morbidity and Mortality in Patients with Severe Heart Failure
Pitt, B., Zannad, F., Remme, W. J., Cody, R., Castaigne, A., Perez, A., Palensky, J., & Wittes, J. (1999) · New England Journal of Medicine · doi:10.1056/nejm199909023411001 · Cited by 9,214
The Transforming Growth Factor-beta Family
Massague, J. (1990) · Annual Review of Cell Biology · doi:10.1146/annurev.cb.06.110190.003121 · Cited by 3,015
The Effect of Spironolactone on Morbidity and Mortality in Patients with Severe Heart Failure
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MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts
Thum, T., Gross, C., Fiedler, J., Fischer, T., Kissler, S., Bussen, M., Galuppo, P., Just, S., Rottbauer, W., Frantz, S., et al. (2008) · Nature · doi:10.1038/nature07511 · Cited by 2,349
TGF-β signaling and the fibrotic response
Leask, A., & Abraham, D. J. (2004) · The FASEB Journal · doi:10.1096/fj.03-1273rev · Cited by 2,319
Desmoulière, A., Geinoz, A., Gabbiani, F., & Gabbiani, G. (1993) · The Journal of cell biology · doi:10.1083/jcb.122.1.103 · Cited by 2,243
Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis
van Rooij, E., Sutherland, L. B., Thatcher, J. E., DiMaio, J. M., Naseem, R. H., Marshall, W. S., Hill, J. A., & Olson, E. N. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0805038105 · Cited by 1,844
LNA-mediated microRNA silencing in non-human primates
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“In this regard, silencing of the liver-specific miR-122 in monkeys recently resulted in a long-lasting lowering of plasma cholesterol levels.(85) A specific inhibitor of miR-122 is the first miRNA-targeted drug that has entered a human clinical trial, in patients infected with Hepatitis C.”
van Rooij, E., Sutherland, L. B., Liu, N., Williams, A. H., McAnally, J., Gerard, R. D., Richardson, J. A., & Olson, E. N. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0608791103 · Cited by 1,507
Molecular Mechanisms of Myocardial Remodeling
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Cited by
Braunwald, E. (2013) · JACC: Heart Failure · doi:10.1016/j.jchf.2012.10.002 · Cited by 730
Ronco, C., Cicoira, M., & McCullough, P. A. (2012) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2012.01.077 · Cited by 422
Galectin-3: One Molecule for an Alphabet of Diseases, from A to Z
Sciacchitano, S., Lavra, L., Morgante, A., Ulivieri, A., Magi, F., De Francesco, G., Bellotti, C., Salehi, L., & Ricci, A. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19020379 · Cited by 377
TGF-β Signaling in Control of Cardiovascular Function
Goumans, M.-J., & ten Dijke, P. (2018) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a022210 · Cited by 360
Heart failure with preserved ejection fraction: from mechanisms to therapies
Lam, C. S. P., Voors, A. A., de Boer, R. A., Solomon, S. D., & van Veldhuisen, D. J. (2018) · European Heart Journal · doi:10.1093/eurheartj/ehy301 · Cited by 355
Metadata
- Authors
- Creemers, E. E., & Pinto, Y. M.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-09-28
- Volume
- 89
- Issue
- 2
- Pages
- 265-272
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W2171820373
- Cited by
- 403
- References
- 81
- FWCI
- 17.17
- Type
- journal article
- Language
- en
- Open access
- closed
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- Creemers, E. E., & Pinto, Y. M. (2011). Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart. Cardiovascular Research. https://doi.org/10.1093/cvr/cvq308
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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