The bone marrow-cardiac axis: role of endothelial progenitor cells in heart failure.
Congestive heart failure (CHF) remains a leading cause of mortality in the developed world. The complex mechanisms involved in the pathophysiology of heart failure (HF) explain some of the limited impact of current recognised therapeutic strategies. There is, therefore, a definite need for new alternative molecular and biological pathways to address the treatment of this condition. Over the past decade, much research has focussed upon identifying the ideal cell type to promote myocardial regeneration. Recently, striking reports suggested the concept that bone-marrow (BM)-derived endothelial progenitor cells (EPCs) participate in cardiac regeneration and function recovery in the setting of progressive HF. The modulation of this complex interaction between the BM and the circulating EPCs could be at the crossroad of multiple therapeutic strategies aimed to protect or restore the myocardium in the setting of the CHF. However, there are uncertainties and unresolved issues regarding the mechanisms possibly responsible for the functional benefits observed in chronic experimental and pre-clinical studies. Hence, the BM-cardiac axis concept has created overwhelming enthusiasm and subsequent scepticism in the field of cardiac repair and regeneration. Further intensive research in basic science and clinical arenas are needed to elucidate the potential association between BM and heart function recovery, particularly in the progression towards advance stages of CHF. In this review, we focus on the importance of the BM-cardiac axis and BM-derived EPCs in the pathophysiology, clinical progression and potential treatment of CHF.
Maltais
Simon
S
Department of Surgery, Université de Montréal, Quebec, Canada.
Perrault
Louis P
LP
Ly
Hung Q
HQ
D002633:Chemotaxis / Q000502:physiology; D042783:Endothelial Cells / Q000502:physiology; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology*; D006412:Hematopoietic Stem Cells / Q000502:physiology*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D011379:Prognosis; D019718:Receptors, CXCR4 / Q000502:physiology; D012038:Regeneration / Q000502:physiology
C527276:CXCR4 protein, human; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D019718:Receptors, CXCR4