Stem cell mobilisation for myocardial repair.
BACKGROUND
The idea that autologous bone marrow derived stem cells (BMCs) can transdifferentiate into cardiomyocytes or vascular cells has been challenged in several scientific reports.


OBJECTIVE
This review summarises conditions for stem cell mobilisation, their use for therapeutic approaches to prevent ischaemic cardiomyopathy after acute myocardial infarction and current clinical trials. Mechanisms for mobilisation and homing of BMCs are discussed.


CONCLUSIONS
The improvement in cardiac function after migration of autologous BMCs to the heart can be explained by their paracrine effects, inducing angiogenesis and preventing ischaemic myocardium from apoptosis. These effects may explain why the number of circulating BMCs is directly correlated with cardiovascular risk and life expectancy. Exercise and hormones are physiological stimuli for the mobilisation of BMCs, whereas cardiovascular risk factors severely reduce their number and functions. Current cardiovascular medications increase the amounts of autologous BMCs.
Ludwig-Maximilians-University, Klinikum Grosshadern, Medical Department I, Marchioninistr. 15, 81377, Munich, Germany.
Stefan
S
Brunner
Markus G
MG
Engelmann
Wolfgang-Michael
WM
Franz
D000818:Animals; D002318:Cardiovascular Diseases / Q000378:metabolism / Q000628:therapy*; D002454:Cell Differentiation; D002986:Clinical Trials as Topic; D003324:Coronary Artery Disease / Q000378:metabolism / Q000628:therapy*; D016207:Cytokines / Q000378:metabolism; D016179:Granulocyte Colony-Stimulating Factor / Q000378:metabolism; D006321:Heart / Q000502:physiology; D006333:Heart Failure / Q000378:metabolism / Q000628:therapy*; D019650:Hematopoietic Stem Cell Mobilization; D006801:Humans; D009203:Myocardial Infarction / Q000378:metabolism / Q000628:therapy*; D009206:Myocardium / Q000473:pathology; D009389:Neovascularization, Pathologic; D013234:Stem Cells / Q000378:metabolism*
D016207:Cytokines; D016179:Granulocyte Colony-Stimulating Factor