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• W2076965382 abstract "Sudden occlusion of a major coronary artery and acute myocardial ischemia lead to rapid death of myocytes and vascular structures in the corresponding region of the heart. In the last 2 years, numerous studies have been performed in an attempt to regenerate dead myocardium after infarction (for review, see Refs. [ 1 Anversa P. Nadal-Ginard B. Myocyte renewal and ventricular remodeling. Nature. 2002; 415: 240-243 Crossref PubMed Scopus (437) Google Scholar , 2 Nadal-Ginard B. Kajstura J. Leri A. Anversa P. Myocyte death, growth and regeneration in cardiac hypertrophy and failure. Circ Res. 2003; 92: 139-150 Crossref PubMed Scopus (423) Google Scholar ]). Promising results have been obtained with several approaches varying from the implantation of smooth muscle cells [ [3] Li R. Jia Z.Q. Rd W. Merante F. Mickle D. Smooth muscle cell transplantation into myocardial scar tissue improves heart function. J Mol Cell Cardiol. 1999; 31: 513-522 Abstract Full Text PDF PubMed Scopus (224) Google Scholar ] to the injection of skeletal myoblasts [ 4 Taylor D.A. Atkins B.Z. Hungspreugs P. Jones T.R. Reedy M.C. Hutcheson K.A. et al. Regenerating functional myocardium: improved performance after skeletal myoblast transplantation. Nat M. 1998; 4: 929-933 Crossref PubMed Scopus (990) Google Scholar , 5 Menasche P. Myoblast transplantation: feasibility, safety and efficacy. Ann M. 2002; 34: 314-315 Crossref PubMed Scopus (42) Google Scholar ] or bone marrow-derived primitive cells [ 6 Orlic D. Kajstura J. Chimenti S. Jakoniuk I. Anderson S.M. Li B. et al. Bone marrow cells regenerate infracted myocardium. Nature. 2001; 410: 701-705 Crossref PubMed Scopus (4667) Google Scholar , 7 Orlic D. Kajstura J. Chimenti S. Limana F. Jakoniuk I. Quaini F. et al. Mobilized bone marrow cells repair the infracted heart, improving function and survival. Proc Natl Acad Sci USA. 2001; 98: 10344-10349 Crossref PubMed Scopus (1928) Google Scholar ]. A fundamental concern in myocardial regeneration has always been whether the replication of myocytes is accompanied by the development of coronary vessels within the infarcted region of the wall. Maturation and survival of myocytes invading the infarct is strictly dependent on the presence of oxygen in the area that is undergoing repair. There are two fundamental prerequisites for successful integration of cells in the ischemic region. New coronary arterioles and capillary structures have to be formed in order to bridge the dead tissue and, ultimately, communicate with the normally perfused vessels of the spared myocardium. Additionally, the newly generated vascular supply has to permeate the engrafted myocytes to preserve their viability, and favor their growth and contractile function. The mechanisms by which these vessels become interconnected with the primary coronary circulation remain to be established. However, the studies from Dr. Kloner’s laboratory on page 607 in this issue of the journal shed some light and raise some interesting hypotheses concerning the ability of locally released humoral factors to promote the formation of coronary vasculature [ [8] Reffelmann T. Dow J.S. Dai W. Hale S.L. Simkhovich B.Z. Kloner R.A. et al. Transplantation of neonatal cardiomyocytes after permanent coronary artery occlusion increases regional blood flow of infracted myocardium. J Mol Cell Cardiol. 2003; 35 (in this issue): 607-613 Abstract Full Text Full Text PDF PubMed Scopus (60) Google Scholar ]. Rather surprisingly, the implantation of neonatal myocytes after infarction led with time to a significant restoration of coronary blood flow in the scarred portion of the ventricular wall. To our knowledge, this observation has no precedent. It is noteworthy that the neogenesis of capillaries was restricted to areas of successful cell transplantation strongly suggesting that a potential link may exist between myocyte and capillary growth." @default.
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• W2076965382 date "2003-06-01" @default.
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• W2076965382 title "Myocardial damage and repair" @default.
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• W2076965382 doi "https://doi.org/10.1016/s0022-2828(03)00116-0" @default.
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