Ischemic heart disease (IHD) is a serious threat to health of the elderly,and endothelial progenitor cells therapy-induced therapeutic angiogenesis can improve vascular reperfusion and functional recovery in ischemic myocardium.Endothelial progenitor cell (EPC) therapy plays an important role in endothelial repair and postnatal angiogenesis.And the concept of EPC therapy has received attention.EPC population is decreased in numbers and in functional activity,which are correlated with age and cardiovascular risk factor.And patients with these backgrounds have less therapeutic benefit.In this review,we will focus on overview of the latest research progressions of characteristic of EPC in the elderly with IHD,and on current studies of EPC-based angiogenesis therapies for providing theoretical basis in the promising clinical treatment.

Objective:To investigate the expression of transcription factor BACH2 on PBMC in patients with coronary artery disease( CAD) and discuss its significance and role.Methods:The circulating levels of BACH2 and TLR4 in PBMC were evaluated by RT-PCR and Western blot separately.Serum levels of signature cytokines of T-helper cells,cytokines and ox-LDL were evaluated by ELISA.The data among groups were analyzed by one-way ANOVA.Correlation between variables were subjected to linear regression analysis.Results:The expression level of BACH2 down-regulated and TLR4 up-regulated significantly in PBMCs of ACS patients had significantly higher concentrations of serum ox-LDL,cytokines of TH1 cells,TH2 cells and TH17 cells and low level of cytokine of Treg cells.Negative correlation exists significantly between BACH2 and TLR4 in patients with CAD and between BACH2 and IFN-γ,IL-4 and IL-17,and between BACH2 and ox-LDL in serum.However, positive correlation exists significantly between BACH2 and TGF-β1.Conclusion:Increased serum concentrations of ox-LDL probably down-regulated the expression of BACH2 in ACS patients by activating TLR4 on PBMC, resulting in promoting production of pro-inflammatory cytokines and suppressing production of anti-inflammatory cytokine and then might cause ACS.