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Circulation. 2007;116:1176-1184
Published online before print August 13, 2007, doi: 10.1161/CIRCULATIONAHA.106.650903
CLINICAL PERSPECTIVE
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(Circulation. 2007;116:1176-1184.)
© 2007 American Heart Association, Inc.

Molecular Cardiology

CLINICAL PERSPECTIVE

Bone marrow (BM)–derived cells are known to have a broad potential to differentiate into various cells in response to physiological cues. It is generally thought that cardiac hypertrophy arises from hypertrophy of cardiomyocytes and proliferation of cardiac fibroblasts, but it remains unknown whether BM-derived cells are involved in this process. We found that BM-derived cells are mobilized and differentiated into cardiomyocytes in the hypertrophied heart of both hypoxia-induced pulmonary hypertension and transverse aortic constriction models. BM-derived cardiomyocytes are observed in a "stressed" chamber–specific manner during the pathogenesis of cardiac hypertrophy. Both cell fusion and transdifferentiation mechanisms are involved in this regeneration process, with fusion possibly being the principal mechanism in response to pressure overload. Moreover, the present results suggest that BM-derived monocytes might play an important role in the formation of perivascular fibrosis via direct differentiation into myofibroblasts, although it is conventionally believed that only resident myofibroblasts contribute to perivascular fibrosis in hypertrophied heart. Our findings suggest that regeneration of cardiomyocytes through enhanced mobilization of BM-derived cells is seemingly beneficial; however, the enhanced differentiation of BM-derived cells into myofibroblasts in the interstitial space may damage cardiac contractile function. Any therapeutic effort to enhance the mobilization of BM cells in cases of heart failure might have both a useful and an adverse effect and would require a cautious approach.


*    Footnotes
 
The online-only Data Supplement, consisting of an expanded Methods section, is available with this article at http://circ.ahajournals.org/cgi/content/full/CIRCULATIONAHA.106.650903/DC1.


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Circulation 2007 116: 1107. [Extract] [Full Text]



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This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Data Supplement
Right arrow All Versions of this Article:
116/10/1176    most recent
CIRCULATIONAHA.106.650903v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Endo, J.
Right arrow Articles by Fukuda, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Endo, J.
Right arrow Articles by Fukuda, K.
Right arrowPubmed/NCBI databases
Medline Plus Health Information
*Pulmonary Hypertension
Related Collections
Right arrow Remodeling
Right arrow Animal models of human disease
Right arrow Hypertrophy
Right arrow Myogenesis
Right arrow Pulmonary biology and circulation
Right arrow Pulmonary circulation and disease
Right arrowRelated Article

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