Abstract:Aim To identify the role of low density lipoprotein receptor (LDLR) on the proliferation and differentiation of CD11b＋ myeloid subsets, particularly CD11b＋Gr-1＋ immature myeloid cells with LDLR deficiency mice; To explore the mechanism of abnormal immune cell reaction in the pathogenesis of atherosclerosis. Methods 6-8 weeks old LDLR－/－ mice and control wild type (WT) C57 mice were fed with normal diet and high-fat diet for 12 weeks. Flow cytometry was used to analyze the subsets of immune cells in peripheral blood, spleen and bone marrow, especially the expressions of CD11b＋Gr-1＋ myeloid immune cell, CD11b＋Ly6C＋ mononuclear macrophage and CD11b＋CD11c＋ dendritic cell. Simultaneously the expression of Lin－Sca-1－CD34＋cKit＋ common myeloid progenitor (CMP) was detected in LDLR－/－ mouse bone marrow. Using ¹²⁵I marker anti-CD11b as a molecular probe, inflammatory microenvironment of LDLR－/－ mice aortic atherosclerotic plaque was monitored noninvasively in vivo. Results (1)Under the condition of normal diet and high-fat diet, LDLR deficiency markedly enhanced the expressions CD11b＋ and CD11b＋Gr-1＋ myeloid cells in peripheral blood and spleen of LDLR－/－ mice. (2)The expression of CD11b＋Ly6C＋ mononuclear macrophages increased in peripheral blood and liver of LDLR－/－ mice; The expression of CD11b＋CD11c＋ dendritic cells increased in the spleen of LDLR－/－ mice. (3)Under normal diet, the percentage of CMP was increased in LDLR－/－ mice bone marrow compared with WT mice, but decreased under high-fat diet. (4)Using CD11b as the molecular target of inflammation, SPECT/CT could be used to monitor the atherosclerotic plaque of LDLR－/－ mouse in real time. Conclusion LDLR deficiency significantly increases the proliferation and mobilization of CD11b＋Gr-1＋ myeloid immune cells, and promotes the differentiation of mononuclear macrophage and maturation of dendritic cell in LDLR－/－ mice. With CD11b＋ myeloid cells as a target, the inflammatory microenvironment of atherosclerotic plaques can be monitored in vivo.

Abstract:Aim To investigate the roles of N-WASP in angiogenesis induced by Chlamydia pneumoniae (C.pneumoniae) infection and its possible mechanism. Methods After proliferation culture, C.pneumoniae infected human vascular endothelial cell (VEC), and immunofluorescence staining confirmed successful infection. The phosphorylation level of N-WASP was detected by Western blot in VEC infected by C.pneumoniae. The effect of N-WASP specific inhibitor Wiskostain on VEC viability was detected by CCK-8. The effect of Wiskostain working concentrations on C.pneumoniae infection rate was detected by immunofluorescence assay. After C.pneumoniae infected VEC with 5 μmol/L Wiskostain pretreatment, capillary tube formation assay was performed to observe the changes of VEC angiogenesis ability. Results Under fluorescence microscope, typical C.pneumoniae inclusions were found in infected VEC cytoplasm. After VEC was infected with C.pneumoniae for 10 and 24 hours, the level of N-WASP phosphorylation was significantly higher than that in the control group. Capillary tube formation assay showed that after VEC was infected with C.pneumoniae for 16 hours, the number of capillary tube node was significantly higher than that in the control group (P＜0.05). After the pretreatment of VECs with Wiskostain, the role of C.pneumoniae infection in promoting the formation of capillary tube node was significantly weakened, and it was almost impossible to form capillary tube structure (P＜0.05). Conclusion C.pneumoniae infection may promote the formation of new blood vessels possibly through N-WASP.

Abstract:Aim To explore the effect of miR-301a on the expression of inflammatory factors in macrophages, from the perspective of microRNA to clarify the pathogenesis of atherosclerosis, then provide a new way of prevention and treatment of atherosclerosis. Methods ApoE－/－ mice was fed with high fat diet to establish atherosclerosis model, the expression of inflammatory factors in the atery were analyzed by real-time PCR. MiR-301a mimic and miR-301a inhibitor were transfected into RAW264.7 cells, the expression of inflammatory factors was analyzed by real-time PCR, the protein level of NF-κB repressing factor (NKRF) was measured by Western blot, the cellular location of p65 was determined by immunofluorescence. Results The level of miR-301a was increased in ateries of ApoE－/－ mice. Overexpression of miR-301a decreased the protein levels of NKRF and increased the mRNA levels of inflammatory factors, p65 was located in nuleus in the RAW264.7 cells transfected with miR-301a mimic. Inhibition of miR-301a increased the protein levels of NKRF and decreased the mRNA levels of inflammatory factors, p65 was located in cytoplasm in the RAW264.7 cells transfected with miR-301a inhibitor. Conclusion MiR-301a regulates the mRNA expression of TNF-α, IL-6 and MCP-1 in RAW264.7 cells via targeting NKRF to regulate the cellular location of p65.

Abstract:Aim To observe the effect of angiotensinⅡ (AngⅡ) on the autophagy of mouse aortic smooth muscle cells and the regulation of autophagy on cell phenotype conversion. Methods Mouse vascular smooth muscle cells were obtained by primary culture, vascular smooth muscle cells were incubated with 10－6 mol/L AngⅡ at different time, Western blot was used to detect the expression of LC3-Ⅱ. Transmission electron microscope was used to observe the autophagic body of different groups. Vascular smooth muscle cells were pretreated with 3-MA, Baf-A1 and then incubated with 10－6 mol/L AngⅡ for 24 h, Western blot was used to detect the expression of LC3-Ⅱ and the contractile phenotype marker (SM22α and SM-α-actin) and synthetic phenotype marker (OPN) of vascular smooth muscle cells in different groups. qRT-PCR was performed to detect the Atg7 mRNA level after transfection with siRNA Atg7. Western blot was performed to detect the expression of LC3-Ⅱ, SM22α, SM-α-actin and OPN to observe the effect of siRNA Atg7 on AngⅡ-induced autophagy and VSMC phenotype conversion. Results AngⅡ stimulated LC3-Ⅱ expression in a time-dependent manner, 3-MA significantly attenuated the AngⅡ-enforced expression of LC3-Ⅱ while Baf-A1 further increased the expression of LC3-Ⅱ. Both 3-MA and Baf-A1 significantly suppressed AngⅡ-stimulated VSMC phenotype conversion. Transfection with siRNA Atg7 remarkably decreased the expression of LC3-Ⅱ stimulated by AngⅡ and suppressed AngⅡ-stimulated VSMC phenotype conversion. Conclusion AngⅡ-stimulated VSMC phenotype conversion may be autophagy-dependent, and inhibition of autophagy significantly suppressed AngⅡ-stimulated VSMC phenotype conversion.

Abstract:Aim To evaluate the effect of sphingosine-1-phosphate (S1P) receptor agonist FTY720 on early diabetic rat myocardial microvascular lesions. Methods Male Spragure-Dawley (SD) rats were divided into three groups:normal control group, diabetic model group, FTY720-treated group (0.001 g/kg per day orally). Diabetic model rats received intraperitoneal injection of streptozotocin (65 mg/kg). The heart tissue structure was estimated by HE staining. The myocardial microvessel density was observed by CD34 immunohistochemistry. The cardiac microvascular endothelial cell apoptosis was analysed by TUNEL and immunofluorescence mapping. Immunohistochemical staining for TGF-β and typeⅠcollagen were observed with respect to collagen content. Western blot analysis was used to investigate VCAM-1, TNF-α, and IL-6 protein expression. Results Multiple random blood glucose≥16.7 mmol/L was as a marker of diabetic model. In this study, the success rate of diabetic rat model was above 85%. Compared with the normal control group, diabetic model rat myocardial microvascular wall was thickened, the expression of VCAM-1, TNF-α and IL-6 was higher (P＜0.05). The expression of VCAM-1, TNF-α and IL-6 in FTY720-treated group was significantly lower than those in diabetic model group (P＜0.05). In diabetic model group, the density of vascular endothelial cells was decreased and the apoptotic index was significantly increased, while FTY720 could reduce the apoptosis and promote the proliferation of endothelial cells. Conclusion FTY720 may play a protective role in myocardial microvascular injury in diabetic rats.

Abstract:Aim To analyze the expression of calcium activated potassium channel (BKCa), phosphorylated extracellular signal regulated kinase 1/2 (p-ERK1/2) and apoptosis in vascular smooth muscle cells (VSMC) from rabbits with atherosclerosis before and after atorvastatin treatment, and to discuss whether atorvastatin-induced VSMC apoptosis in rabbits with atherosclerosis is associated with BKCa upregulation and ERK signaling pathway inhibition. Methods Experimental rabbits were divided into normal group, atherosclerosis group and atorvastatin group. Tissue samples were taken and rabbit atherosclerotic lesions were observed by HE staining, TUNEL assay was used to measure the apoptosis of VSMC, qPCR and Western blot were performed for detection of rabbit aortic BKCa KCNMB1 mRNA and p-ERK1/2 protein, respectively. Results In atherosclerosis group, the intima of thoracic aorta was significantly thickened, showing typical atherosclerotic lesions. The apoptotic index of VSMC in atorvastatin group was significantly higher than that in normal group and atherosclerosis group (36.51%±1.53% vs. 6.80%±1.08% and 27.83%±1.36%, P＜0.01). The KCNMB1 mRNA expression in atherosclerosis group was significantly lower than that in normal group (105.12±5.50 vs. 147.33±5.76, P＜0.01), while the KCNMB1 mRNA expression in atorvastatin group was significantly higher than that in atherosclerosis group (116.43±6.92 vs. 105.12±5.50, P＜0.01). Phosphorylation of ERK1/2 in atorvastatin group was lower than that in atherosclerosis group (0.90±0.14 vs. 3.48±0.91, P＜0.01). Conclusion Atorvastatin can induce VSMC apoptosis, which may be related to the upregulation of KCNMB1 gene expression and the inhibition of phosphorylation of ERK signaling pathway.

Abstract:Aim To explore the effect of adiponectin (APN) on acute alcohol induced myocardial injury in mice and related mechanism, and to provide experimental basis and new ideas for the prevention and treatment of acute alcoholic myocardial injury and alcoholic cardiomyopathy. Methods 8 week old C57BL/6J male mice were randomly divided into normal control group (n＝10) and normal model group (n＝15). 8 week old male SPF homozygous adiponectin knockout (APN－/－) mice were randomly divided into APN－/－ control group (n＝10) and APN－/－ model group (n＝15). Model groups were given intraperitoneal injection of ethanol 3 g/(kg·d), control groups received normal saline intraperitoneal injection. 4 groups of mice were normal feeding, drinking water. After 3 days, the indicators were monitored:the general condition of mice was observed, serum lactate dehydrogenase (LDH) and N-terminal B type natriuretic peptide (NT-proBNP) were detected, cardiac structure and function index were detected by mouse heart ultrasonic machine, myocardial cell apoptosis was detected by TUNEL and the activity of Caspase 3 was determined, myocardial tissue HE staining and Masson staining were prepared, myocardial tissue homogenate reactive oxygen species (ROS) content, malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were detected, Western blot was used to detect NADPH oxidase 2 (NOX2) protein expression in myocardial tissue. Results Compared with normal control group, ejection fraction of normal model group decreased significantly (P＜0.01); serum LDH and plasma NT-proBNP concentration of normal model group were increased by 1.98 times, 5.13 times (P＜0.01); HE staining and Masson staining showed myocardial structure and muscle fiber changes, collagen fibers increased, collagen volume fraction (CVF) value increased 2.63 times in normal model group (P＜0.01); the activity of Caspase 3 in myocardial tissue increased 2.58 times (P＜0.01), positive myocardial cell apoptosis increased 12.67 times by TUNEL in normal model group (P＜0.01); ROS content and MDA content in myocardium were increased by 1.68 times, 2.87 times (P＜0.01), SOD activity increased 2.92 times in normal model group (P＜0.01); the expression of NOX2 protein increased 1.87 times in normal model group (P＜0.01). Compared with control group, the above indicators in APN－/－ model group were significantly increased (P＜0.01). Compared with normal group, serum LDH and plasma NT-proBNP concentration were increased by 1.30 times, 1.25 times in APN－/－ model group (P＜0.01); HE and Masson staining showed the myocardial structure and muscle fiber changes, collagen fibers increased, CVF value increased by 1.55 times in APN－/－ model group; the activity of Caspase 3 in myocardial tissue increased 1.66 times (P＜0.01), the myocardial cell apoptosis ratio was 1.64 times higher in APN－/－ model group (P＜0.01); ROS content and MDA content in myocardium were increased by 1.42 times, 1.39 times (P＜0.01), SOD activity decreased 28% in APN－/－ model group (P＜0.01), the expression of NOX2 protein increased 1.44 times in APN－/－ model group (P＜0.01). Conclusion Adiponectin can reduce acute alcoholic myocardial injury in mice, and its mechanism may be related to the inhibition of NOX2 protein expression and the effect of anti-oxidative stress.

Abstract:Aim To study the expression of miR-142-5p in atherosclerosis tissues and its effect on human macrophage apoptosis. Methods Rat atherosclerosis model was constructed, qRT-PCR was used to detect the expression of miR-142-5p in atherosclerotic tissues. 50 μg/L ox-LDL stimulated human macrophage, vascular smooth muscle cell, endothelial cell for 24 h, qRT-PCR was used to detect the expression of miR-142-5p in the cells. Target gene prediction software was used to predict the target gene of miR-142-5p, dual luciferase reporter gene was used to identify the target gene. Cells were transfected with miR-142-5p mimic, mimic control, miR-142-5p inhibitor, inhibitor control into macrophage, Western blot and qRT-PCR were used to to detect the expression of miR-142-5p on target gene, the effect of miR-142-5p and target gene on the apoptosis of macrophages was detected by flow cytometry. Results MiR-142-5p expression was up-regulated in atherosclerotic tissues compared with normal tissue, and the difference was significant (P＜0.01).After stimulation with ox-LDL, the levels of miR-142-5p in vascular smooth muscle cells and endothelial cells did not change significantly compared with before stimulation, but the level of miR-142-5p in the macrophages was significantly higher than that before stimulation (P＜0.01). Predicting the target gene of miR-142-5p was transforming growth factor-β2 (TGF-β2). The luciferase activity was the lowest after transfection with miR-142-5p mimic and TGF-β2. The expression of TGF-β2 protein and mRNA in miR-142-5p mimic group was significantly decreased compared with mimic control group (P＜0.01), the expression of TGF-β2 protein and mRNA in miR-142-5p inhibitor group was significantly higher than that in inhibitor control group (P＜0.01), the apoptosis rate of miR-142-5p mimic group was significantly higher than that of mimic control group (P＜0.01), the apoptosis rate of TGF-β2 siRNA group was significantly higher than that of siRNA control group (P＜0.01). Conclusion MiR-142-5p was over expressed in atherosclerosis tissues, and miR-142-5p could promote the apoptosis of human macrophages by regulating the target gene TGF-β2.

Abstract:Aim To observe the changes of Toll-like receptor 4 (TLR4) and tumor necrosis factor-α(TNF-α) in patients with acute coronary syndrome (ACS) and its correlation with the severity of coronary artery disease, and to explore its clinical significance. Methods 60 patients with ACS, 20 patients with stable angina pectoris (SAP) and 20 patients with normal control group were selected according to clinical manifestation, ECG and the results of coronary angiography. The ACS patients included 30 patients with acute myocardial infarction (AMI) and 30 patients with unstable angina pectoris (UAP). The degree of coronary artery lesion was evaluated according to the improved Gensini score. In the control group, coronary artery angiography was performed to exclude coronary artery disease. The levels of TLR4 in peripheral blood of 100 patients were detected by flow cytometry, and the concentration of TNF-α in serum were detected by ELISA. Results The levels of TLR4 and TNF-α in ACS group were significantly higher than those in control group and SAP group (P＜0.01), while TLR4 levels were not significantly different between AMI group and UAP group, SAP group and control group (P＞0.05). The levels of TLR4 and TNF-α in patients with ACS decreased but there were significantly lower than those in SAP group and control group (P＜0.05). There was a positive correlation between the expression of TLR4 and TNF-α in blood and the Gensini score of coronary artery lesion (r＝0.715, P＜0.01; r＝0.333, P＜0.01). Conclusions The level of TLR4 in peripheral blood of patients with ACS significantly increased, and the secretion of TNF-α increased. It was suggested that TLR4 and TNF-α concentrations in peripheral blood of patients with ACS were related to the progression of ACS. The levels of TLR4 and TNF-α in peripheral blood were closely related to the degree of coronary artery disease, and after PCI treatment, the expression of TLR4 and TNF-α decreased significantly. It is suggested that myocardial perfusion therapy may improve the coronary artery inflammation.

Abstract:Aim To investigate the relativity of apolipoprotein A5 gene (ApoA5) c.553G/T polymorphism in exon 4 with hyper total cholesterolemia (HTC) in Zunyi Han Nationality. Methods c.553G/T polymorphism of 101 HTC patients and 118 healthy individuals were tested by polymerase chain reaction and restriction fragment length (PCR-RFLP) assay. Results The genotype frequency of ApoA5 gene c.553G/T showed statistically difference between patients group and normal groups (P<0.05), and the distribution of ApoA5 c.553T gene in HTC group was significantly higher than normal group (P<0.05), therefore it had independent effect on HTC (OR=4.5,5%CI:1.269～17.296,P=0.020). It has more optical clinical significance comparing different blood lipid index ratio than one blood lipid index. Conclusion There was relativity between ApoA5 gene c.553G/T polymorphism and HTC in Zunyi Han Nationality. The c.553T gene was an independent risk factor for HTC.

Abstract:Aim To investigate the clinical factors which influence platelet aggregation function in patients after percutaneous coronary intervention(PCI). Methods A retrospective study was conducted on 266 patients with coronary heart disease which underwent PCI. All patients were treated with clopidogrel and aspirin dual anti-platelet therapy and standard medication. Patients were divided into 0%~29%, 30%~49%, 50%~69%, 70%~100% groups according to the adenosine diphosphate(ADP)-induced platelet aggregation rate(PAR). The CYP2C19 genotypes, general clinical information, lab indexes and coronary artery lesions after PCI were compared among the four groups. Risk factors of elevated PAR were explored by logistic regression analysis. Results There were significant differences in gender ratio, age, brain natriuretic peptide(BNP), CYP2C19 genotype among four groups of PAR(P<0.05). Logistic regression analysis revealed that female(OR=2.713, P=0.027), higher BNP(OR=1.002, P=0.007), slow metabolism genotype(OR=5.159, P<0.001) were risk factors for PAR≥50%; and female(OR=5.716, P=0.008), slow metabolism genotype(OR=3.149, P=0.049) was independent risk factor for PAR ≥70%. Conclusion Majority of patients with PAR<50% were fast metabolism genotype, and patients with slow metabolism genotype usually had PAR more than 50%; CYP2C19 polymorphism had strong impact to PAR. In addition, female and higher BNP might be risk factors of elevated PAR in patients with coronary heart disease after PCI.

Abstract:Aim To quantitatively evaluate the residual lesions of patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI) using the residual SYNTAX score, and to investigate the prognostic impact of this score to predict long-term servival rate after PCI. Methods 782 patients with ACS undergoing PCI between January 2014 to May 2015 from the Heart Center of the First Hospital of Lanzhou University were included. The baseline SYNTAX score(bSS) and residual SYNTAX score (rSS) were calculated before and after PCI, patients were divided into tow groups based upon rSS:rSS=0 complete reascularization group(CR), rSS＞0 incomplete reascularization group (IR). IR group was divided into the following three groups:0＜rSS≤4 low-risk group, 4＜rSS≤8 moderare-risk group,rSS＞8 high-risk group. Major adverse cardiac cerebrovascular events(MACCE) rates (all-cause mortality, myocardial infarction,repeat revascularization and stroke) and cardiac death were followed-up in 14 months. Results 676 cases were followed-up, 106 cases were lost to follow-up. (1) Compared with CR group, each group with IR had higher incidence of 3-vessel coronary artery disease(CAD) and higher bSS, especially the patients of the high-risk group with rSS＞8,they had higher incidence of 3-vessel CAD, hypertension and higher bSS than other three groups(P＜0.05). (2) Compared with CR group and low-risk group, the moderare-risk group and high-risk group had a higher MACCE rate, all-cause mortality, cardiac death rate and repeat reascularization rate(P＜0.05), and there was no statistical difference between CR group and low-risk group(P＞0.05). (3)No event Kaplan Meier survival curves showed that the three groups with IR had lower survival curves than CR group, and the no event survival curve of the high-risk group with rSS＞8 was the lowest(P＜0.001). (4)Multivariable logistic regression analysis showed rSS was a strong independent predictor of varieties of adverse cardiovascular events at 14 months of patients with ACS undergoing PCI, including MACCE rate, all-cause mortality, cardiac death rate and repeat reascularization rate, the ROC curve of rSS and the end point events showed rSS had a good prediction ability to the events described above, and there was no obvious correlation between rSS and postoperative myocardial infarction. Conclusion The rSS quantitatively evaluate residual lesions of the patients with ACS undergoing PCI, it is an independent predictor of varieties of cardiovascular adverse events after PCI for 14 months, and the patients with rSS＜4 have a better prognosis than the patients with rSS＞4, and the patients with rSS＞8 have a poor prognosis.

Abstract:Aim The aim of this study was to establish the accuracy of transthoracic echocardiography (TTE) in diagnosis of acute aortic dissection type Stanford A. Methods A total of 35 cases of acute aortic dissection type Stanford A were retrospectively analyzed, who underwent both transthoracic echocardiography and CTA. Results The diagnostic accuracy of TTE and CTA of acute aortic dissection type Stanford A were 91.3% and 100%, respectively. However, TTE could show aortic valve abnormalities, heart function, pericardial effusion. Conclusion TTE is a reliable method for diagnosis of acute aortic dissection type Stanford A. The pivotal role of TTE in the evaluation of the patients with suspected acute type A aortic dissection in emergency room setting.

Abstract:Aim To evaluate the mid-term prognostic value of serum growth differentiation factor-15(GDF-15) in acute coronary syndrome(ACS). Methods Totally 95 consecutive patients with acute coronary syndrome were included. Their baseline levels of serum growth differentiation factor-15 (GDF-15) were determined using enzyme-linked immunosorbent assay (ELISA). The patients were divided into low concentration group and high concentration group according to median value of GDF-15. The mid-term survival rate and major adverse cardiovascular events (MACE) during the follow-up period were observed using Kaplan-Meier survival analysis method. Receiver operating characteristic (ROC) curve was measured to evaluate the mid-term prognostic value of serum growth differentiation factor-15 in acute coronary syndrome. Results There were 95 cases in the whole study including four deaths. The mean follow-up was 33.76±6.29 months. The serum growth differentiation factor-15 level in acute coronary syndrome patients were 921.56±462.20 ng/L. Survival analysis showed that survival rate in patients with high level of serum GDF-15 was statistically lower than low level of serum group (P=0.039). The area under the ROC curve is 0.853(SE=0.074,P=0.017,95%CI 0.708~0.998)in evaluation of mid-term survival rate and 0.805(SE=0.068,P=0.000,95%CI 0.672~0.938)in predicating MACE. Conclusion GDF-15 level predicted mid-term prognosis in acute coronary syndrome. As a new biochemical marker, GDF-15 is of clinical significance in evaluating risk stratification and mid-term prognosis in acute coronary syndrome.

Abstract:Aim To investigate the relationship between 24-hour ambulatory blood pressure variability (BPV) and renal dysfunction in the elderly. Methods In the third physical examination for Kailuan Group, the method of cluster sampling was adopted to randomly draw 3064 retired employees(≥60 years old), with 24-hour ambulatory blood pressure monitoring. Finally, 1382 participants with integral data were recruited into the survey. The elderly were divided into four groups by quartile of the standard deviation of systolic blood pressure (SSD). Biochemical index was recorded. The estimated glomerular filtration rate (eGFR) was calculated. The effect of SSD on kidney function was analyzed using rank correlation analysis and stepwise linear regression model. Results Among 1382 participants (67.16±5.86 years old), 905 individuals were male and 477 were female. Rank correlation analysis confirmed that there was a significant negative correlation between eGFR levels and 24hSSD, daytime SSD, nighttime SSD. Stepwise linear regression analysis indicated that there was a significant negative linear correlation between eGFR and 24hSSD, daytime SSD after adjustment for other risk factors. Conclusion There was a significant negative linear correlation between eGFR levels and 24hSSD, daytime SSD.

Abstract:Lipoprotein lipase (LPL) degradation is one of the important ways to regulate the level of LPL. Recently, it has been found that LPL degradation is regulated by a variety of related proteins, the process of LPL degradation mainly includes two parts:intracellular degradation and extracellular degradation. The intracellular degradation of LPL means a large amount of newborn LPL which were transferred to the lysosome for degradation via the related proteins. The extracellular degradation of LPL means mature LPL which were re-uptaked or transported into the cell under the action of the related proteins, and then gathered into lysosomal for degradation. This article will review the LPL in the process of LPL protein synthesis, transportation and biological functions, and then elucidate the relationship between its degradation and metabolic syndrome.

Abstract:Atrial fibrillation, often associated with coronary artery disease, requires a combination of anticoagulation and antiplatelet therapy to reduce the risk of stroke and cardiovascular events. However, the combination of antithrombotic therapy increase the risk of bleeding, and need to weigh the advantages and disadvantages of antithrombotic therapy. At present, there is still lack of large-scale clinical evidence. This review summarizes the current evidences published and recommendations in consensus and guidelines at home and abroad.

Abstract:Fibroblast growth factor 21 (FGF21) is involved in the regulation of glucose and lipid metabolism, and is closely related to obesity, diabetes, metabolic syndrome, nonalcoholic fatty liver disease and other diseases or pathological processes. The present studies show that FGF21 can antagonize myocardial ischemia and ischemia reperfusion injury, play a significant role in myocardial protection, and its mechanism may be related to anti-apoptosis of cardiomyocyte, anti-inflammation, anti-oxidative stress, regulation of myocardial cell energy metabolism and mitochondrial function, and so on.This review summarizes the research progress of myocardial protective effect of FGF21 and its mechanism.

Abstract:Endothelial cells are considered as important organs for metabolism and secretion, and play an importmant role in regulating the function of blood vessel. The development of multiple cardio-cerebrovascular diseases, such as atherosclerosis, hypertension and diabetic vascular complications, is closely related to endothelial injury. The mechanisms of vascular endothelial cell injury have not yet fully clarified. A large number of studies have shown that mechanisms of endothelial cell injury are mainly related to inflammatory reaction and oxidative stress. Endothelial progenitor cells play an important role in repairing endothelial injury. A variety of chemical drugs and traditional Chinese medicine play the role of endothelial protection by means of reducing induced factors, inhibiting inflammation reaction and oxidative stress, delaying endothelial cell aging and other ways.

Abstract:Ischemic disease is one of the serious diseases that is harm to human health, which mainly includes ischemic cerebrovascular disease, ischemic heart disease, ischemic disease of lower extremities. Progenitor cells and stem cells are pluripotent cells with self-replicating ability. Under certain conditions, they are able to differentiate into a variety of cells. According to the developmental stages of stem cells, it is classified into embryonic stem cells and somatic stem cells. Although embryonic stem cells have abilities of differentiating into any cell, the ethics dispute makes its study difficult. Compared with embryonic stem cells, somatic stem cells can not only avoid the ethical controversy, but also have no immune rejection after transplanting. Therefore, this essay focuses on the application of stem cells and progenitor cells in ischemic disease. In recent years, the research on the application of progenitor cells and stem cells in this kind of disease has increased, and aroused wide attention, which provides us with a new approach to the treatment of ischemic diseases.