Circulation. 2007;116:1176-1184
Published online before print August 13, 2007, doi: 10.1161/CIRCULATIONAHA.106.650903
Published online before print August 13, 2007, doi: 10.1161/CIRCULATIONAHA.106.650903
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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.
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Footnotes |
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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.
Related Article:
Circulation 2007 116: 1107.
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