Abstract
Systemic available circulating cells play a role in cardiac maintenance and ameliorate cardiac recovery and repair after myocardial infarction. However, only a small number of cells will be incorporated during cardiac damage. Cell mobilization, homing to the ischemic myocardium and engraftment are complex processes depending on many adhesion molecules, proteases, chemokines and their receptors. Physiologic and pathophysiologic circumstances, cytokines, chemokines and certain drugs are able to influence these processes. For cardiovascular regeneration, understanding how mobilization and homing of blood derived cells is regulated and can be modulated as well as identification of cell populations able to regenerate the heart or reduce damage after myocardial infarction is essential for the development of successful cell based therapies.
Keywords: Blood cells, cytokines, homing, left ventricular ejection fraction, mobilization, myocardial infarction, Cell Trafficking, Cardiac Regeneration, Ischemic heart disease, Primary percutaneous coronary intervention, heart failure, cellular therapy, dysfunctional part, physiological conditions cardiomyocytes, Meta-analyses, peripheral blood, bone marrow derived cells, conventional therapy, mature lymphocytes, macrophages, coronary artery obstruction, Cardiac wound healing, necrosis, cardiomyocyte shrinkage, inflammatory phase, influx, lymphocytes, plasma cells, tensile strength, maturation, remodeling phase acellular, chamber dilatation, cell death, vascularization, sex-mismatched transplantations, cardiac chimerism, X-Y mismatch heart, parabiosis experiments, quail embryo, adenomas, tumor vascular endothelium, SUBPOPULATIONS FOR CARDIAC REGENERATION, ischemic, adipose tissue, mononuclear cells, paracrine mechanism, pro-angiogenic factors, Hematopoietic Stem Cells, growth factors, cell infusion, in-stent reocclusion, restenosis, infusion, ventricular ejection, Endothelial Progenitor Cells, monocytic origin, ATP-binding, SP cells, tendon, cartilage, culture plastic, murine, ischemia-reperfusion model, progenitor cell, CELL MOBILIZATION, cardiac function, damage reduction, physiologic conditions, hematooncologic diseases, hypoxia inducible factor-1α, neutrophil elastase, cysteine protease, metalloproteinase, antigen-1, erythroid, cleavage of stromal cell membrane, ligand, plasma soluble, placental growth factor, Adenoviral mediated plasma, nitric oxide synthase, insulin-like growth factor, high tensile strength, Activation by Chemoattractants, EPC-integrin binding, activated by monocyte chemoattractant protein 1, Cell arrest, homed cells, adenovirus, hematologists, chemotaxis of progenitor cells, N-terminus cleavage, hyperlipidemia, ibesartan, blood EPC counts, anti-hypertensive drugs, co-internalize, angina pectoris, dilated cardiomyopathy, neovascularisation capacity, chemotactic response, atherosclerotic plaques
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