Abstract:Aim To study whether erythropoietin(EPO)has effect on bone marrow KDR+ stem cells and the possible mechanism in mice with acute myocardial infarction(AMI).Methods Acute myocardial infarction mice were established by cryoinjury.Sixty male mice were randomly divided into four groups after cryoinjury:EPO group,AMD3100 inhibition group,control group,sham surgery group.The changes of KDR positive cells in peripheral blood were determined by flowcytometry.Immunohistochemisty was used to detect capillary density of peri-infarct area in 2 and 4 weeks after surgery.Results Compared with EPO group,the number of KDR positive cells in peripheral blood decreased in AMD3100 inhibition group(2.88%±0.67% vs 0.28%±0.13%,P><0.05).Two and four weeks after acute myocardial infarction modeling,the capillary density in EPO group was significantly higher than that in AMD3100 inhibition group and control group(P><0.05).But only 2 weeks after surgery,the capillary density in AMD3100 inhibition group was higher than that in control group(P><0.05).Conclusion EPO can effectively mobilize KDR+ stem cells from bone marrow to peripheral blood,which increased capillary density in peri-infarct area in mice with acute myocardial infarction.The effect can be completely restrained by AMD3100,which suggested that EPO may mobilize KDR+ cells in bone marrow to peripheral blood by SDF-1α/CXCR4 axis.

Abstract:Aim To explore the effects of advanced oxidation protein products(AOPP)on expressions of stromal cell-derived factor-1α(SDF-1α)in ECV304 cells and the signal pathway that mediated the effects.Methods AOPP-BSA was made from bovine serum albumin(BSA)and sodium hypochlorite.After different time treated with AOPP-BSA,the expressions of SDF-1α mRNA in ECV304 cells were measured by reverse transcription polymerase chain reaction(RT-PCR)and the expressions of SDF-1α protein and the levels of phosphored-p38 mitogen-activated protein kinase(MAPK)were analyzed by Western Blotting.In inhibition test SB₂03580,the special inhibitor of p38MAPK of different concentrations were added into ECV304 culture media for 1 hour,then the cells were treated with AOPP-BSA for 12 hours,at last the protein levels in supernatant were measured by enzyme linked immunosorbent assay(ELISlA).Results Compared with control group,the expressions of SDF-1α mRNA and protein in ECV304 cells increased significantly after incubated with 200 μmol/L AOPP-BSA for 2 hours(P><0.05).The expression of SDF-1α mRNA peaked after 6 hours(P><0.01)and decreased gradually until there was no differentiation at 24 hours.Expression of SDF-1α protein increased in a time-dependent manner and peaked at 24 hours(P><0.01).After 15 minutes the levels of phosphored-p38MAPK increased significantly(P><0.05).When the p38MAPK pathway was blocked by SB₂03580(0.1 μmol/L,1 μmol/L,10 μmol/L),the promoting effects of AOPP-BSA on expressions of SDF-1α protein in ECV304 cells were significantly inhibited(618.85±60.12,500.98±69.47,359.97±59.81,P><0.05 or 0.01).Conclusion AOPP induced the expression of SDF-1α from ECV304 cells,p38MAPK signal pathway is an important pathway that mediated the effects.

Abstract:Aim To investigate the role of peroxisome proliferator-activated receptor-γ(PPARγ)signal transduction pathway in the up-regulation of the expressions of acyl-CoA:cholesterol acyltransferase 1(ACAT1)and discuss the mechanism of macrophages-derived form cell formation induced by visfatin.Methods THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate(PMA)for 48 h,then exposed to visfatin and PPARγ activator rosiglitazone.The lipid droplet contents were observed by Oil red staining.The expressions of PPARγ and ACAT1 mRNA and protein were determined by reverse transcriptase-polymerase chain reaction(RT-PCR)and Western blotting respectively.The contents of total cholesterol(TC)and free cholesterol(FC)were detected by enzyme fluorescence analysis.Results Compared with the control group,the lipid droplet contents were increased,the expressions of PPARγ mRNA and protein were down-regulated,the expressions of ACAT1 mRNA and protein were up-regulated,and the contents of cholesterol ester(CE)were increased in visfatin groups.Compared with the visfatin group,the expressions of ACAT1 mRNA and protein were down-regulated in rosiglitazone groups.Conclusion The up-regulation of ACAT1 expression was induced by visfatin via PPARγ signal transduction pathway,which induced foam cell formation.

Abstract:Aim To evaluate the effects of dietary iodine intake on the development of atherosclerosis in mice and to further investigate the association between iodine and cardiovascular disease.Methods Female C57BL/6 mice,weaning 1 month and weighing around 16 g,were randomly divided into five groups according to the iodine intakes:severe iodine deficiency(SID),mild iodine deficiency(MID),normal iodine(NI),10-fold high iodine(10 HI)and 50-fold high iodine(50 HI).All the mice were fed by high fat high cholesterol low iodine fodder(HFHCLI,iodine content is 20～40 μg/kg)and drank deionized water containing different concentrations of potassium iodide including 0 μg/L(SID),196.08 μg/L(MID),326.79 μg/L(NI),3 856.21 μg/L(10 HI)and 19 542.5 μg/L(50 HI)respectively.Eight months later,all the animals were sacrificed.Serum thyroid hormones(total T4 and total T3)were measured by radio immunoassay.The levels of triglyceride(TG),total cholesterol(TC),high density lipoprotein cholesterol(HDLC),low density lipoprotein cholesterol(LDLC)in the serum were detected enzymatically by automatic analysis.The extent of lesion development in the proximal aorta or aortic root was observed by hematoxylin-eosin staining on the paraffin-embeded tissue slides.Real-time PCR was applied to detect the expressions of intercellular adhesion molecule-1(ICAM-1)mRNA and vascular cell adhesion molecule-1(VCAM-1)mRNA in aorta and low-density lipoprotein receptor(LDLR)mRNA in liver.Results(1)The levels of thyroid hormones(total T4 and total T3)were distinctively decreased in SID and MID,especially in SID,compared with NI group(P><0.01 or P><0.05).(2)The levels of TG,TC and LDLC in SID and LDLC in MID were obviously higher than that in NI group(P><0.01).In contrast,the levels of TC in both 10 HI and 50 HI groups were statistically lower than NI group(P><0.01).(3)Pathological changes showed that in the tunica intima,sub-endothelial space was obviously wider with lipids deposition in NI.In MID and SID,sub-endothelial space was progressively wider and foam cells were found in regional area with some lipids around them,called fatty streak formation.In 10 HI and 50 HI group,sub-endothelial space was just slightly wider and the staining was pale.(4)Both ICAM-1 and VCAM-1 mRNA in the aorta tissues were highly expressed in SID than NI group(P><0.01).Similarly,the expression level of ICAM-1 mRNA in MID group was higher than NI group(P><0.01).In contrast,much lower expressions of these adhesion molecules were detected in 50 HI group compared with NI group(P><0.01 or P><0.05).The expression levels of LDLR mRNA in liver in SID and MID group were much lower while higher in 10 HI and 50 HI group than NI group(P><0.01 or P><0.05).Conclusion Dietary iodine intake could influence the development of atherosclerosis in mice fed by lipid-enriched diets by regulating thyroid function,the metabolism of serum lipids and the gene expression in liver.Iodine deficiency can have deleterious effects on the cardiovascular system,and a higher iodine intake may benefit it.

Abstract:Aim To explore the effects of allicin on cholesterol excretion and expression of ABCG5 and ABCG8 in Caco-2 cells.Methods Caco-2 cells were randomly divided into control group,cholesterol group,cholesterol plus allicin group,and allicin group.After treatment,oil O staining,high performance liquid chromatography and western blot were performed.Results Cholesterol treatment of Caco-2 cells showed increased intracellular lipid droplet and cholesterol contents compared with control group(P><0.05).However,Allicin significantly decreased lipid droplet and cholesterol contents in cholesterol-treated Caco-2 cells,increased efflux of cholesterol from the cells into the medium.Furthermore,allicin up-regulated the expression of ABCG5 and ABCG8 in Caco-2 cell.Conclusion These results suggest that allicin contributes to excretion of cholesterol from Caco-2 cell,which is related to up-regulation of ABCG5 and ABCG8 expression.

Abstract:Aim To explore the inhibition of aldosterone(ALD)on proliferation of human umbilical vein endothelial cells(HUVEC)and its mechanism.Methods MTT was used to measure the proliferation.Flow cytometry assay(FCM)was applied for the detection of the apoptosis;Vascular Endothelial Growth Factor(VEGF)mRNA and VEGF protein were measured by semiquantitative RT-PCR and Western blot,respectively.Results ①Proliferation of HUVEC was inhibited by ALD in a dose-dependent manner,the cell viability of HUVEC decreased gradually.②However,when the concentration of ALD was above 800 μg/L,HUVEC were resistant to ALD.After the cells were incubated with ALD(800 μg/L)for 24 h.The rate of apoptosis in the HUVEC could reach 26.5%±3.3%.③The expression of VEGF mRNA and VEGF protein in HUVEC were decreased after it was incubated with ALD.Conclusion ALD can induce apoptosis and inhibit proliferation of HUVEC through changing the expression of VEGF.

Abstract:Aim To observe and compare the expression of heme oxygenase-1 and-2 in the brain of high fat and diabetic mouse.Methods Heme oxygenase expression was detected by reverse transcription polymerase chain reaction(RT-PCR),Western Blotting and immunochemistry.Results More significant heme oxygenase-1 mRNA and protein expression were observed both in the brain of high fat mouse and diabetic mouse,and the mRNA expression were 1.63 times and 1.60 times of those of control group.Elevated expression of heme oxygenase-2 were observed only in the brain of diabetic mouse,and the quantitative evaluation showed that heme oxygenase-2 protein was increased 1.83-fold in the diabetic group compared with that of control group.Conclusion Heme oxygenase was over-expressed in the brain of diabetic mouse.

Abstract:Aim To determine whether the proapoptotic effect of proprotein-convertase cubtilisin/kexin 9(PCSK9)is related to its effect on Caspase-3 activation by bioinformatics analysis.Methods HUVEC-12 were incubated with 80 mg/L oxidized low density lipoprotein(ox-LDL)for 24 h,and groups of blank control,transfection reagent control,negative control,and 80 nmol/L PCSK9 siRNA+80 mg/L ox-LDL were established.Apoptosis rate was measured by flow cytometry.Western blotting and ELISA were used to measure Caspase-3 protein expression and activity,respectively.Bioinformatics methods were used to compare PCSK9,Caspase-8 and Caspase-9,in order to find the similarity of sequence and whether a common conservative motif existed.Results An inhibitory effect of PCSK9 siRNA on both expression and activity of Caspase-3 was observed.The sequence similarity of PCSK9,Caspase-8 and Caspase-9 was 22.14%,there was a similar second structure in C-terminal of the three proteins,the content of helix,strand,turn and coil was nearly the same in PCSK9 and Caspase-9,the profile of PCSK9 and Caspase-9 was similar,and there was common cleft in their abdomen,this cleft may be related to their similar enzyme activity.Conclusion There are similar motif in PCSK9 and Caspase-9.The proapoptotic capacity of PCSK9 is related to its effect on Caspase-3 activation.

Abstract:Aim To investigate the action of estrogen receptor in Genistein upregulating the expression of endothelial nitric oxide synthase(eNOS)in endothelial cells.Methods Human umbilical vein endothelial cells were exposed to medium or oxide low density lipoprotein(ox-LDL)(100 mg/L)in the presense or absence of estrogen antagonists ICI182780(1 μmol/L)or/and actinomycin D(5 mg/L)for 0.5 hour,then were treated with Genistein(100 nmol/L)for 24 hours.The mRNA expression of eNOS was detected by real-time PCR,the protein expression of eNOS was determined by Western Blotting.Results ox-LDL downregulated the expression of eNOS mRNA and protein(P><0.05 vs that of basal level);Genistein upregulated the expression of eNOS mRNA and protein(P><0.05 vs that of ox-LDL-treated group),furthermore,the increase can be inverted by estrogen antagonists ICI182780 or actinomycin D(P><0.05).Conclusion Genistein could upregulate the expression of eNOS,which is associated with estrogen receptor regulating genes transcription.

Abstract:Aim To investigate the effects of fasudil hydrochloride on the injury of human umbilical vein endothelial cells(HUVEC)induced by angiotensinⅡ(AngⅡ)which influence on the expression of Rho associated kinase(ROCK)and phospho-myosin light chain(P-MLC).Methods HUVEC were incubated in vitro and treated with AngⅡ,AngⅡ+specific blocker(Y-27632),AngⅡ+fasudil hydrochloride for different time.Cell activities were detected by MTT method.Morphous and distribution changes of F-actin were observed by immunofluorescence,expression of ROCK and P-MLC were measured by Western Blotting.Results Compared with control group,AngⅡ had significant inhibitory effect on endothelial cells vigor(P><0.01),furthermore,these effects were dose-dependent(P><0.01)in the other three groups.Morphous and distribution changes of F-actin by imunofluorescence,compared with control group,the rupture of stree fibers constructed by F-actin,deformation and digitation of HUVEC were exhibited.Compared with AngⅡ group,expression of ROCK and P-MLC in the specific blocker group and the drug group were remarkably restrained(P><0.01),but higher than the control group(P><0.01).Conclusion Fasudil hydrochloride can protect the cytoskeletal of HUVEC which were induced by AngⅡ,through obviously controlling the expression of ROCK and P-MLC in the Rho/Rho kinase signaling pathways,thus weakened the damage in cytoskeletal.

Abstract:Aim To investigate the correlations of atherogenic index of plasma with serum lipids of hyperlipidaemia patients and their thrombotic risk factors.Methods Serum lipids and homocysteine,uric acid,6-Keto-PGF1,TXB₂,FⅦ and other biochemical parameters were detected by standard methods in 100 cases of hyperlipidaemia and 109 controls.The atherogenic index of plasma(AIP)was calculated,and the correlation of AIP,UA,Hcy with other thromboplastic risk factors were analyzed by multiple linear regression respectively.Results Compared to controls,the levels of TC,TG,BMI,AIP,GLU,LDLC,FⅦ,PGI2 and non-HDLC were significantly increased(P><0.01),and the levels of TXB₂ and TXB₂/PGI2 were decreased(P><0.01)in the hyperlipidaemia.The index of AIP was significantly and positively correlated with BMI,DBP,GLU,TG,UA,non-HDLC,SBP,FⅦ and Hcy and negatively correlated with HDLC(P><0.05).Serum homocysteine was significantly and positively correlated with age,SBP,DBP,UA and negatively correlated with HDLC(P><0.01).The level of UA was significantly and positively correlated with TG,BMI,TXB₂(P><0.05 or P><0.01)and negatively correlated with HDLC(P><0.01).BMI was positively correlated with TG,DBP,UA(P><0.01)and negatively correlated with HDLC(P><0.01).Conclusion The levels of AIP,PGI2,non-HDLC and FⅦ were significantly increased in hyperlipidaemic patients compared to control subjects.TC and TG were correlated with various thrombotic risk factors.The index of AIP was corresponding closely to BMI,DBP,GLU,TG,UA,non-HDLC,SBP,FⅦ and Hcy.AIP could accurately evaluate the risk of hyperlipidaemia patients,AIP was closely related to homocysteine,high uric acid hematic disease and high level of FⅦ,which formed the atherosclerosis risk factors.

Abstract:Aim To assess the possible association between cellular repressor of the interleukin-17(IL-17F)His161Arg polymorphism and myocardial infarction(MI)in a Han Chinese population.Methods We conducted a case-control association study on a cohort of 1 068 unrelated MI patients and 985 age and sex-matched controls to investigate the association between the IL-17F His161Arg polymorphism and MI risk in a Chinese Han population.Results The genotype frequencies of TT,TC and CC in the IL-17F His161Arg polymorphism were 76.3%,17.9% and 5.8% in MI group,75.8%,16.6%,and 7.6% in the controls respectively(P>0.05).The T allele frequency of IL-17F His161Arg polymorphism allele in MI cases and controls were 85.3% and 84.2% respectively(P>=0.33).Further stratification analysis by gender or age and analysis of clinical features in relation to myocardial infarction also yielded negative results(P>0.05).Conclusion This study indicates the IL-17F His161Arg polymorphism is unlikely to be a major contributor to the pathogenesis of MI.

Abstract:Aim To assess the association between the length of(GT)n repeats in the heme oxygenase-1(HO-1)gene promoter and the susceptibility for coronary heart disease(CHD)of Chaoshan population.Methods 300 patients with CHD and 182 control subjects with sex and age matching were collected.Amplification and labeling of PCR products for capillary electrophoresis were performed to genotype.(GT)n repeat polymorphism was classified into short(n≤25 for S allele)and long(n>25 for L allele)alleles.Results Allelic and genotypic frequency did not differ significantly between CHD patients and control subjects.However,there were interaction between genotype and smoking(OR was 1.790,95%CI was 1.110-2.886),hypertension(OR was 1.552,95%CI was 1.045-2.304)and diabetes(OR was 1.727,95%CI was 1.018-2.928).Specially,the SL+LL genotype had the highest risk(OR was 2.517,95%CI was 1.206-5.253).Conclusion Our findings indicated that longer(GT)n repeat allele in HO-1 promoter is a susceptibility marker of CHD with risk factors in Chaoshan population.

Abstract:Aim To evaluate the relationship between unstable plaques and the levels of high-sensitivity C-reactive protein(hs-CRP)and interleukin-6(IL-6)by intravascular ultrasound(IVUS).Methods 38 patients diagnosed with coronary heart disease by IVUS examination were chosen.Eight patients by IVUS examination were found with no coronary artery stenosis as control group,30 cases by IVUS examination were found with coronary artery stenosis as coronary heart disease group,including 18 cases with unstable angina pectoris(UAP)and 12 cases with stable angina(SAP).Serum hs-CRP and IL-6 levels of all patients were detected.Results 38 patients had varying degrees of intimal thickening.IVUS showed that 30 cases of coronary heart disease patients had different types of atherosclerotic plaque.Serum hs-CRP and IL-6 levels in UAP group were significantly higher than that in SAP group and control group.Serum hs-CRP and IL-6 levels were higher in unstable plaque group than those in stable plaque group.Conclusion Serum hs-CRP and IL-6 was significantly higher in the UAP patients.It prompted that the levels of hs-CRP and IL-6 could reflect the instability degree of atherosclerotic plaque.

Abstract:Aim To observe the effects of degradable coating and non-degradable coating with sirolimus-eluting stents on systemic and local levels of high sensitivity C-reactive protein(hs-CRP)and interleukin-6(IL-6).Methods Consecutive 118 patients with unstable angina pectoris(UAP)with a stent implanted were involved and divided into non-degradable coating group(n=65)and degradable coating group(n=53).The serum concentrations of hs-CRP and IL-6 were determined before and immediately,at 48 hours,7 days,and 9 months after coronary intervention,and local levels in coronary were determined before and immediately,at 9 months after stent implantation.Results There was no significant difference in clinical and angiographic baseline characteristics and basic serum hs-CRP and IL-6 concentrations between the two groups.The local IL-6 levels increased immediately after stent implation in both group.The circulatory serum hs-CRP and IL-6 levels at 48 hours and 7 days after stenting were significantly higher in both group compared with baseline.When compared between the two groups,there was no significant difference of hs-CRP and IL-6 levels at 48 hours,7 days,and 9 months after stenting both in systemic and in local levels.Conclusion It seemed that degradable coating and non-degradable coating with sirolimus-eluting stents may display similar effects on systemic and local inflammation.

Abstract:Aim To investigate the changes of serum heat shock protein 70(HSP70)levels and its related factors in patients with coronary heart disease(CHD).Methods 66 patients with CHD and 21 healthy controls(non-CHD group)were enrolled in this study.66 patients with CHD were divided into two groups:acute coronary syndrome group(composed of acute myocardial infarction group(AMI,n=23)and unstable angina pectoris group(UAP,n=23)),stable angina pectoris group(SAP,n=20).Serum HSP70 levels were determined by ELISA.Meanwhile high sensitive C-reactive protein(hs-CRP),fasting blood sugar(FBS),total cholesterol(TC),triglyceride(TG),low density lipoprotein cholesterol(LDLC),high density lipoprotein cholesterol(HDLC),and peripheral white blood cell(WBC)count were measured.Results Serum HSP70 levels in ACS group(4.72±2.01 μg/L)were significantly higher than those in SAP group(2.33±1.44 μg/L)and non-CHD group(2.41±0.96 μg/L;P><0.01).But the difference of serum HSP70 levels between SAP group and non-CHD group was not statistically significant(P>0.05).Among patients with CHD,serum HSP70 levels in AMI group(5.94±1.98 μg/L)were much higher than those in UAP group(3.49±1.10 μg/L;P><0.01),and serum HSP70 levels in UAP group were much higher than those in SAP group(2.33±1.44 μg/L;P><0.01).Serum HSP70 levels were associated positively with WBC(r=0.337,P><0.01),CK-MB(r=0.653,P><0.01)and hs-CRP(r=0.658,P><0.01),but negatively with HDLC(r=-0.211,P><0.05)among all the subjects.Conclusion Serum HSP70 levels may be valuable to predict the unstable plaque and evaluate the severity of ACS.

Abstract:Aim To observe the protective effects of Edaravone injection and Captopril in patients of myocardial ischemia-reperfusion injury.Methods 68 eligible patients of CPB heart surgery in the year of 2009~2010 were selected and divided randomly and averagely into treatment group(n=34)and control group(n=34).The treatment group will be given Edaravone injection and Captopril.The control group will just be given Edaravone injection.Then the researcher will observe the incidence of arrhythmia,changes of heart rate and detect the contents of CK-MB,cTnI,artery angiotensionⅡ(AngⅡ)and MDA,SOD and NO by mining the radical artery after 120 minutes of the reperfusion.Results The content of CK-MB,cTnI,AngⅡand MDA in treatment group was lower obviously.However,there is obvious increase in content of SOD and NO.Compared with the control group,the differences were statistically significant for the research(P><0.05).Conclusion Edaravone injection and Captopril will reduce the incidence of arrhythmia and heart rate,increase the activities of myocardial SOD and NO.It can reduce the MDA production and the myocardial ischemia reperfusion injury and effectively protect the myocardial function.

Abstract:Aim To evaluate condition of lipid metabolism in the population of north areas of Qinling Mountains in Shaanxi Province,and describe the epidemiological characteristics of people with dyslipidemia.Methods According to 2007 China adult dyslipidemia guidelines,a prevalence survey with stratified random sampling method in 3298 persons was carried out.Results The detection rate of dyslipidemia was 33.54%,standardized rate was 32.11%.The incidence rates of hypercholesterolemia was 8.13%,standardized rate was 7.48%.The incidence rates of hypertriglyceridemia was 16.89%,standardized rate was 15.40%.The incidence rate of lower high density lipoprotein(HDL)was 19.77%,standardized rate was 19.72%.The prevalence of dyslipidemia had no difference between urban and rural areas,but there was significant difference in sex.The prevalence of dyslipidemia,hypercholesterolemia and hypertriglyceridemia had trend of increasing with age growing.Smoker and drinker had significantly higher rate of dyslipidemia.Diabetes and hypertension groups also showed a higher rate of dyslipidemia.After Logistic analysis on dyslipidemia,the risk factors included gender,body mass index(BMI),hypertension,diabetes and education.Conclusion The prevalence of dyslipidemia in the north areas of Qinling Mountains in Shaanxi Province is relatively high.Prevention and treatment of blood fat should be made according to the gender,hypertension,diabetes,obesity condition and education level.

Abstract:Coronary artery bypass grafting(CABG)is a highly effective method in the treatment of coronary heart disease(CAD).However,its effectiveness is impeded by the limited life expectancy of vein grafts,which are the most common types of conduits used.Many reports presented follow-up angiographic data on large cohorts of patients,demonstrating that approximately one-half of vein grafts fail within 10 to 15 years of surgery and that graft failure is associated with worse clinical outcomes.Therefore,understanding the venous-specifc pathophysiological and molecular mechanisms of vein graft adaptation is important for clinical vein graft management.This overview describes the normal development and regulation of vessel,compares the differences between artery and vein,introduces the adaptive response of vein graft to the arterial environment during the post-surgical process and its molecular mechanism,and discusses various therapeutic prospects.

Abstract:Vascular calcification is an active,cell-regulated process,characterized by the deposition of hydroxyapatite crystal in vascular wall,resulted from high-calcium/phosphate-environment,up-regulation of mineralization inducers and down-regulation of mineralization inhibitor in local or systemic sites.In this process,the protective system against vascular mineralization is exhausted,and mesenchyma,such as vascular smooth muscle cells(VSMC),lose the intrinsic phenotypes,but gain the osteogenic phenotypes.Consequently,mineralized cells release some lipid vesicles,which have two forms at least in vascular wall,such as matrix vesicle and apoptosis body.Lipid vesicles provide appropriate nucleating micro-environments for vascular calcification,and vascular elastin provides the bracket structure for hydroxyapatite deposition.So,under the condition that the balance between calcium deposition(mediated by osteoblast-like cells)and calcium absorption(mediated by osteoclast-like cells)is disrupted,ectopic calcification of vascular intima,media or aortic valve may be developed.Intervention on the mechanisms and risk factors of vascular calcification may bring some beneficial effects on the reverse and regression of vascular calcification.In particular,up-regulation on the number and activity of osteoclasts or osteoclast-like cells in calcification lesion may be a more efficient therapeutic strategy.However,it will be a difficult problem in future how to coordinate the relation between normotopic bone formation and ectopic calcification absorption because of calcification paradox in bone-vascular axis.

Abstract:After the injury of vascular endothelial,bone marrow-derived endothelial progenitor cell can be mobilized into the peripheral circulation,home to ischemic areas or sites of vascular damage,inducing endothelial cell proliferation,migration or differentiating into functional mature endothelial cell to promote the reendothelization of the damaged vessels.So it may become a new tool for treatment of cardiovascular disease.However,the signaling pathway that regulates endothelial progenitor cell proliferation,migration,differentiation and other biological characteristics needs to be thoroughly researched,which is not only difficult,but also hot in this area.This review will focus on the research regulation of endothelial progenitor cell signaling pathway.