Ann Thorac Surg 2009;88:1921-1922. doi:10.1016/j.athoracsur.2009.08.029
© 2009 The Society of Thoracic Surgeons
Original Articles: Adult Cardiac
Invited Commentary
Ian M.C. Dixon, PhD
ICVS, Department of Physiology, University of Manitoba, Room 3038, SBGH Research Centre, 351 Tache Ave, Winnipeg, MB, R2H 2A6 Canada
(Email: idixon{at}sbrc.ca).
Oliver Wendell Holmes, the American physician and humorist offered the following quote: "The great thing in the world is not so much where we stand, as in what direction we are moving." This is certainly true of the field of extracellular matrix biology, especially in the context of heart disease. Despite the pioneering work of Weber, Borg, Caulfield, and others, the role of the cardiac matrix was somewhat ignored as a player in the pathogenesis of heart failure until the past decade. This view is now changing, and in 2008, Doris Taylor (from the University of Minnesota) used a perfused rat heart to create decellularized cardiac matrix constructs, and she has demonstrated the critical role of the matrix in organizing reintroduced cardiac myocytes to produce a bioartificial functioning cardiac pump de novo [1]. This underscores the importance of the matrix in the normal heart. By extension, one might suggest that disruption of the normal matrix deposition in maladaptive cardiac hypertrophy, secondary to hypertension or large myocardial infarction, may then be causal to cardiac pump dysfunction if the existing myocytes are subject to subtle rearrangement or displacement within the remodeled matrix, or both of these conditions.
The exciting work by Stansfield and coworkers [2] highlights the expression of periostin in hypertrophied hearts. Periostin is normally expressed during cardiac development and may be re-expressed after myocardial injury. The current study highlights the novel discovery of a link between periostin protein and extracellular matrix in the aortic-arch banded mouse model, as well as in patients receiving left ventricular assist device therapy prior and subsequent to treatment. The positive correlation and temporal connection to periostin expression and fibrosis in both mouse and humans is remarkable, particularly after pressure normalization in the experimental model. The parallelism in upregulation and downregulation of periostin and fibrotic cardiac events is of considerable interest, and it supports a causal role for periostin in stimulating cardiac matrix production, presumably by resident ventricular myofibroblasts. Indeed, the role of periostin may extend beyond stimulation of myofibroblasts and also include cardiac myocytes, as Kühn and colleagues [3] have recently shown that after myocardial infarction, periostin may cause the induction of proliferation in border zone cardiomyocytes in the infarct border zone, resulting in improved cardiac function. Thus, periostin may be held up as a putative therapeutic target for heart failure. Nonetheless, this avenue should be approached with caution, given the important new results published in this issue of The Annals of Thoracic Surgery.
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References
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- Ott HC, Matthiesen TS, Goh SK, et al. Perfusion-decellularized matrix: using nature's platform to engineer a bioartificial heart Nat Med 2008;14:213-221.[Medline]
- Stansfield WE, Andersen NM, Tang R-H, Selzman CH. Periostin is a novel factor in cardiac remodeling after experimental and clinical unloading of the failing heart Ann Thorac Surg 2009;88:1916-1922.[Abstract/Free Full Text]
- Kühn B, del MF, Hajjar RJ, et al. Periostin induces proliferation of differentiated cardiomyocytes and promotes cardiac repair Nat Med 2007;13:962-969.[Medline]
Related Article
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Periostin Is a Novel Factor in Cardiac Remodeling After Experimental and Clinical Unloading of the Failing Heart
- William E. Stansfield, Nancy M. Andersen, Ru-Hang Tang, and Craig H. Selzman
Ann. Thorac. Surg. 2009 88: 1916-1921.
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[Full Text]
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