Implantation of bone marrow stem cells reduces the infarction and fibrosis in ischemic mouse heart
M Kudo, Y Wang, MA Wani, M Xu, A Ayub… - Journal of molecular and …, 2003 - Elsevier
Journal of molecular and cellular cardiology, 2003•Elsevier
Myocardial infarction may cause sudden cardiac death and heart failure. Adult cardiac
myocytes do not replicate due to lack of a substantive pool of precursor, stem, or reserve
cells in an adult heart. Ventricular myocytes following myocardial infarction are replaced by
fibrous tissue and this leads to congestive heart failure in severe cases. Anversa et al.
described that resident cardiac stem cells are present in the heart, and can repair the
damaged mycardium by myocyte regeneration. Recent findings suggest the feasibility of …
myocytes do not replicate due to lack of a substantive pool of precursor, stem, or reserve
cells in an adult heart. Ventricular myocytes following myocardial infarction are replaced by
fibrous tissue and this leads to congestive heart failure in severe cases. Anversa et al.
described that resident cardiac stem cells are present in the heart, and can repair the
damaged mycardium by myocyte regeneration. Recent findings suggest the feasibility of …
Myocardial infarction may cause sudden cardiac death and heart failure. Adult cardiac myocytes do not replicate due to lack of a substantive pool of precursor, stem, or reserve cells in an adult heart. Ventricular myocytes following myocardial infarction are replaced by fibrous tissue and this leads to congestive heart failure in severe cases. Anversa et al. described that resident cardiac stem cells are present in the heart, and can repair the damaged mycardium by myocyte regeneration. Recent findings suggest the feasibility of cardiac repair using cell transplantation. However, it remains controversial which cell types are the best for cell transplantation in the ischemic heart. In this study, we demonstrate that cultured bone marrow stromal cells (MSCs) and Lin– bone marrow cells upon transplantation differentiate into myocytes and endothelial cells in the ischemic heart, eventually reducing both infarct size and fibrosis.
Elsevier
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