Abstract:The incidence rate and mortality of cardiovascular disease are increasing. Myocardial ischemia and myocardial infarction are the main causes. Cardiopulmonary endurance reflects the fitness of cardiopulmonary function and the tolerance to maximum exercise intensity. Cardiopulmonary endurance is one of the five vital signs of human body, which can be used to evaluate the risk of cardiovascular disease. Cardiopulmonary exercise test (CPET), as a new objective noninvasive detection technology of cardiopulmonary integration, can predict the potential pathophysiological changes of patients earlier. The data interpretation of CPET is relatively complex and not widely used, so it has great potential in clinical application. At present, CPET application fields include disease diagnosis, condition and prognosis risk assessment, exercise prescription formulation and so on. It is in line with the mainstream of cardiac rehabilitation to evaluate and diagnose the early risk of cardiovascular disease with CPET.

Abstract:As a recently identified family member of the heme-containing peroxidases in cardiovascular system, vascular peroxidase 1 (VPO1) can utilize NADPH oxidase (NOX)-derived hydrogen peroxide (H₂O₂) to produce hypochlorous acid (HClO) then greatly amplify the oxidatice stress, and it is implicated in the pathogenesis of several cardiovascular diseases such as hypertension, atherosclerosis, myocardial infarction and pulmonary arterial hypertension. This review aims to summarize the role and potential mechanism of VPO1-mediated oxidative stress in cardiovascular diseases.

Abstract:Aim To study the mechanism of benzo(a)pyrene (BaP) affecting autophagy in human umbilical vein endothelial cell (HUVEC). Methods HUVECs were treated with BaP (2.5,5, 10 μmol/L) for 24 h. The degradation of autophagosome and its contents, the expressions of target proteins microtubule-associated protein 1 light chain 3 (LC3), sequestosome 1 (p62), Beclin-1, autophagy-related protein 5 (Atg5), Atg7, Atg12, cathepsin B (CTSB), cathepsin D (CTSD), syntaxin 17 (STX17), lysosomal associated membrane protein 2 (LAMP2), the number and function of lysosomes, and the phosphorylation levels of related upstream key regulatory proteins serine-threonine protein kinase (Akt), extracellular regulated protein kinase (ERK) and transcription factor EB (TFEB) were detected respectively by indirect immunofluorescence, Western blot, acridine orange staining and monodansyl cadaverine staining.Results In HUVEC of BaP exposure group, the test results showed that:(1)The level of LC3 puncta and the ratio of LC3Ⅱ/LC3Ⅰ increased, the expressions of key autophagy initiation proteins (Beclin-1, Atg5, Atg7 and Atg12) increased, and the phosphorylation of Akt protein decreased significantly; (2)The levels of p62 puncta and p62 protein increased significantly; (3)The number of lysosomes increased, accompanied by the increased expressions of lysosomal characteristic hydrolases (CTSB, CTSD), and the phosphorylation levels of ERK and TFEB increased accordingly; (4)The key proteins STX17 and LAMP2 regulating the fusion of autophagy and lysosome decreased. Conclusion BaP inhibits the normal autophagic flux of HUVEC by reducing the expression levels of STX17 and LAMP2.

Abstract:Aim To investigate whether N-acetylcysteine (NAC) can protect endothelial cells from high glucose induced injury by inhibiting JAK2 /STAT3 signaling pathway. Methods Human umbilical vein endothelial cells (HUVEC) were pretreated with different concentrations of NAC in vitro, and the optimal concentration of NAC was selected to reduce the cytotoxicity of HUVEC induced by high glucose. HUVEC were pretreated with the best concentration of NAC, afterwards ,the survival rate of HUVEC was measured by CCK-8, the morphological changes of endothelial cell apoptosis were detected by Hoechst33258 nuclear staining, the protein expression of JAK2/STAT3 signaling pathway was detected by Western blot, and the level of intracellular reactive oxygen species was detected by DCFH-DA, the levels of intercellular cell adhesion molecule-1 (ICAM-1), nuclear factor-κB (NF-κB), tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), IL-6 and IL-8 were detected by ELISA, and the changes of mitochondrial membrane potential were detected by fluorescence probe JC-1. Results NAC pretreatment of HUVEC for 30 min could significantly reduce the injury induced by high glucose, increase the cell survival rate, reduce the number of apoptosis, decrease the expression of cleaved Caspase-3, decrease the accumulation of intracellular reactive oxygen species and the loss of mitochondrial membrane potential (P＜0.01). NAC can inhibit the up-regulation of p-JAK2 and p-STAT3 expression induced by high glucose (P＜0.01), inhibit the inflammatory response induced by high glucose, and decrease the levels of inflammatory factors such as ICAM-1, NF-κB, TNF-α, IL-1β, IL-6 and IL-8 (P＜0.01). Conclusion NAC can protect HUVEC from high glucose induced injury by inhibiting JAK2/STAT3 signaling pathway.

Abstract:Aim To observe whether the effect of curcumin on lipid uptake of human hepatoma cell line HepG2 is related to kinesin family member 16B (KIF16B), and to explore the lipid-lowering mechanism of curcumin. Methods (1)The HepG2 cells cultured in vitro were divided into control group (curcumin concentration was 0) and 0,0, 40 μmol/L curcumin treatment groups, and CCK8 method was used to detect cell viability to determine the appropriate concentration of curcumin. (2)The HepG2 cells cultured in vitro were divided into blank control group, negative control group, rosuvastatin (positive drug) group and curcumin group. Cholesterol detection kit was used to detect the content of cholesterol in HepG2 cells; The uptake of DiI-labeled low density lipoprotein (DiI-LDL) was observed by fluorescence microscope; The protein expressions of KIF16B and low density lipoprotein receptor (LDLR) were detected by Western blot; The fluorescence co-localization of KIF16B and LDLR was observed by laser confocal microscope. Results 25 μmol/L curcumin did not affect the growth of HepG2 cells. Compared with the negative control group, the levels of total cholesterol and free cholesterol in HepG2 cells were significantly increased, the uptake of DiI-LDL by cells was significantly increased, the expressions of KIF16B and LDLR proteins in the cells were significantly increased, and the fluorescence co-localization of KIF16B and LDLR proteins in the cells was significantly increased in the curcumin group (P＜0.05). Conclusion The increase of LDL lipid uptake and LDLR expression caused by curcumin acting on HepG2 cells is related to the interaction between KIF16B and LDLR.

Abstract:Aim To investigate the effect of obstructive sleep apnea syndrome (OSAS) on peripheral blood C1q level in patients with unstable angina pectoris (UAP) and its correlation with platelet aggregation rate (PAR) after percutaneous coronary intervention (PCI). Methods 182 patients with UAP who underwent PCI treatment in Beijing Anzhen Hospital from July 2018 to July 2019 were continuously selected. All patients underwent polysomnography. Patients with apnea hypopnea index (AHI)≥15 were taken as the OSAS group (n＝92), and patients with AHI＜15 were taken as the control group (n＝90). Serum C1q level and adenosine diphosphate induced PAR were detected. The relationship between AHI, serum C1q and PAR was analyzed. Results The serum C1q level in OSAS group was significantly higher than that in control group (176.00 (174.8,9.26) mg/L vs 174.50 (167.5,0.76) mg/L, P＝0.030). One month after PCI, PAR in OSAS group was significantly higher than that in control group ((51.36%±19.34%) vs (42.56%±22.23%), P＝0.007). Spearman correlation analysis showed that AHI and serum C1q were positively correlated with PAR (r＝0.219, P＝0.003; r＝0.634, P＜0.001). Multivariable linear regression analysis showed that AHI and serum C1q were independent factors influencing the increase of PAR after PCI (P＝0.036; P＜0.001). Conclusions Serum C1q is significantly increased in UAP patients with OSAS. AHI and C1q are the influencing factors of high platelet reactivity in UAP patients with OSAS one month after PCI.

Abstract:Aim To investigate the predictive value of levels of serum peroxisome proliferator activated receptor γ coactivator-1α (PGC-1α) mRNA and irisin in patients with acute ischemic stroke. Methods 161 patients with acute ischemic stroke were divided into non secondary hemorrhagic transformation (HT) group (97 cases) and secondary HT group (64 cases) according to the presence or absence of secondary HT. The levels of PGC-1α mRNA and irisin in serum were detected by real-time quantitative PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) respectively; Triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDLC), high density lipoprotein cholesterol (HDLC) and creatinine were detected by automatic biochemical analyzer. The correlation between serum PGC-1α mRNA, irisin levels and blood lipids in patients with secondary HT to acute ischemic stroke was analyzed, the predictive value of serum PGC-1α mRNA and irisin levels was analyzed by receiver operating characteristic (ROC) curve, and the influencing risk factors were explored. Results The levels of PGC-1α mRNA, irisin and TG were lower in secondary HT group than those in non secondary HT group, while the level of HDLC in secondary HT group was higher than that in non secondary HT group (P＜0.05); The serum PGC-1α mRNA and irisin of acute ischemic stroke patients with secondary HT were positively correlated with TG level (P＜0.05), and negatively correlated with HDLC level (P＜0.05); The area under the curve (AUC) of serum PGC-1α mRNA and irisin levels in predicting secondary HT in patients with acute ischemic stroke was 0.865 and 0.893, the specificity was 85.9% and 87.5%, and the sensitivity was 74.2% and 82.5%, respectively; The AUC of the combined diagnosis was 0.960, the specificity was 89.1%, and the sensitivity was 87.6%; In addition, PGC-1α mRNA and irisin were protective factors of secondary HT in patients with acute ischemic stroke (P＜0.05), and HDLC was an independent risk factor (P＜0.05). Conclusion The levels of serum PGC-1α mRNA and irisin in patients with secondary HT are significantly lower than those without HT, which may be of great value in predicting the occurrence of HT.

Abstract:Aim To investigate the correlation between serum Nesfatin-1, heat shock protein 60 (HSP60) and lower extremity vascular disease (LEVD) in patients with type 2 diabetes (T2DM). Methods A total of 120 T2DM patients were selected and divided into two groups according to whether the lower extremity vascular ultrasound examination was combined with LEVD, 62 cases in the LEVD group, 58 cases in the non-LEVD group, and the other fifty healthy subjects were selected as the control group, the serum Nesfatin-1 and HSP60 levels of all subjects were measured, and the relationship between serum Nesfatin-1, HSP60 levels and LEVD in T2DM patients was analyzed. Results The serum Nesfatin-1 level was significantly lower in the LEVD group than that in the non-LEVD group, and the HSP60 level was significantly higher than that in the non-LEVD group (P＜0.05); the serum Nesfatin-1 level in patients with different LEVD grades decreased with the increase of the disease grade, and the HSP60 level increased with the increase of lesion grade (P＜0.05); Pearson correlation analysis showed that body mass index (BMI), waist to hip ratio (WHR), glycosylated hemoglobin (HbA1c), fasting blood glucose (FPG), fasting insulin (FINS), insulin resistance index (HOMA-IR), low-density lipoprotein cholesterol (LDLC), alanine aminotransferase (ALT), serum creatinine (SCr), blood urea nitrogen (BUN) levels were negatively correlated with Nesfatin-1 level, and positively correlated with HSP60 levels; high-density lipoprotein cholesterol (HDLC) levels were positively correlated with Nesfatin-1 level, and negatively correlated with HSP60 level (P＜0.05); multivariate stepwise Logistic regression analysis showed that Nesfatin-1, HSP60 was independent influencing factors of T2DM patients with LEVD (P＜0.05). Conclusions Serum Nesfatin-1 level in T2DM patients combined with LEVD were significantly reduced, and HSP60 levels were significantly increased, and changed with the severity of the disease. They are independent factors affecting LEVD. Early detection of serum Nesfatin-1 and HSP60 levels can help prevent LEVD in time.

Abstract:Aim To investigate the changes of serum neurofilament-light (NF-L), thrombospondin-1 (TSP-1) levels in patients with craniocerebral injury,and analyze their predictive value for the prognosis of patients with craniocerebral injury. Methods 106 craniocerebral injury patients were selected,according to Fisher CT grade the patients were divided into 1 ~ 2 grade group(47 cases) and 3 ~ 4 grade group(59 cases), according to the Glasgow coma scale (GCS) the patients were divided into light coma group(12~15 points, 34 cases), medium coma group (7~11 points, 49 cases), and heavy coma group(＜7 points,23 cases), according to the injury after 30 days Glasgow outcome scale (GOS) the patients were divided into poor prognosis group(GOS scores 1~3,8 cases) and good prognosis group(GOS scores 4~5,8 cases). Another 103 healthy volunteers (control group) were selected. Serum NF-L and TSP-1 levels were detected by enzyme linked immunosorbent assay. Spearman rank correlation analysis was used to analyze the correlation between serum NF-L, TSP-1 level and Fisher CT grade, GCS scores, GOS scores in craniocervical injury patients. Logistic regression analysis was used to analyze the risk factors affecting the prognosis of patients with craniocerebral injury. The receiver operating characteristic (ROC) curve was used to analyze the value of serum NF-L and TSP-1 levels in predicting the prognosis of patients with craniocerebral injury. Results Serum NF-L, TSP-1 levels in craniocerebral injury group were higher than control group(P＜0.05); The serum NF-L,TSP-1 levels in Fisher CT 3~4 grade group were higher than that in 1 ~ 2 grade group(P＜0.05); And the serum NF-L,TSP-1 levels in heavy coma group were higher than medium coma group and light coma group(P＜0.05); The serum NF-L,TSP-1 levels in medium coma group were higher than light coma group(P＜0.05); The serum NF-L and TSP-1 levels in the poor prognosis group were higher than those in the good prognosis group(P＜0.05). Spearman rank correlation analysis showed that serum NF-L and TSP-1 levels were positively correlated with Fisher CT grade(r_s=0.2,0.593, P＜0.05), and negatively correlated with GCS score and GOS score(r_s=－0.589, －0.693; －0.629, －0.617, P＜0.05). Logistic regression analysis showed that Fisher CT grade, GCS scores, NF-L, and TSP-1 were correlated with the prognosis of patients with craniocerebral injury (P＜0.01). ROC curve analysis showed that the area under the curve (AUC) of serum NF-L and TSP-1 to predict the prognosis of patients with craniocerebral injury were 0.3,0.836 respectively, and the AUC combined with NF-L and TSP-1 was 0.937, which was higher than that of NF-L and TSP-1 alone(P＜0.05). Conclusion Serum NF-L and TSP-1 are significantly increased in patients with craniocerebral injury, and the NF-L and TSP-1 levels are closely related to the severity and prognosis of craniocerebral injury, and can be used as a reference index for prognosis assessment.

Abstract:Aim To investigate the effect of renin-angiotensin system inhibitor (RASI) on long-term prognosis in patients with coronary heart disease (CHD) after contrast-associated acute kidney injury (CA-AKI). Methods A total of 1 526 patients with CHD diagnosed by coronary angiography and postoperative CA-AKI in Guangdong Provincial People's Hospital from January 2008 to December 2018 were included in this study. They were divided into RASI group (n＝984) and non-RASI group (n＝542) according to whether they took RASI or not. The primary end point was long-term all-cause death. Baseline clinical data were compared between the two groups. Kaplan-Meier method and COX regression analysis were used to evaluate the effect of RASI on long-term prognosis. Results The proportion of β-receptor blockers and statins used in the RASI group was higher than that in the non-RASI group (P＜0.01). During the median follow-up period of 4.75 years (quartile 2.82 years, 6.67 years), 332 patients died, and the all-cause mortality was 21.76%. Kaplan-Meier survival analysis showed that the mortality of RASI group was lower than that of non-RASI group (P＝0.001). Univariate and multivariate COX regression analysis showed that RASI treatment after discharge was significantly negatively correlated with all-cause death (P＝0.001, P＝0.034), and RASI was an independent protective factor for long-term all-cause death. Conclusions RASI is an independent protective factor for the long-term prognosis of CHD patients after CA-AKI. Long-term use of RASI therapy can reduce the all-cause death in patients with CHD and CA-AKI.

Abstract:Aim To explore the predictive value of combined detection of red blood cell distribution width (RDW) and N-terminal pro-brain natriuretic peptide (NT-proBNP) for acute kidney injury (AKI) after acute myocardial infarction (AMI). Methods A total of 110 patients with AMI admitted to Beijing Hospital of Integrated Traditional Chinese and Western Medicine from July 2018 to may 2020 were enrolled for retrospective study. Patients were divided into AKI group (n＝29) and non-AKI group (n＝81) according to whether AKI occurred within one week after admission.The levels of RDW and NT-proBNP in AKI group and non-AKI group were detected and compared. The clinical data of the two groups were collected, and the risk factors of AKI after AMI were analyzed by Logistic regression model. The correlation between RDW and NT-proBNP in AMI patients with AKI was analyzed by Pearson linear correlation analysis. The receiver operating characteristic curve (ROC) was drawn and the area under curve (AUC) was determined. The predictive value of RDW, NT-proBNP alone and combined detection for AKI after AMI was analyzed. Results The proportions of three vessel lesion and diuretic use in AKI group were 58.62% and 44.83% respectively, which were significantly higher than 27.16% and 18.52% in non-AKI group (P＜0.01). Uric acid (UA), blood urea nitrogen, serum creatinine, RDW and NT-proBNP levels in AKI group were significantly higher than those in non-AKI group, while estimated glomerular filtration rate (eGFR) was significantly lower than that in non-AKI group (P＜0.01). The results of Logistic regression model showed that the number of lesion, diuretic use and UA, eGFR, RDW, NT-proBNP were the risk factors of AKI in patients with AMI (P＜0.05). RDW was positively correlated with NT-proBNP (r＝0.693, P＜0.05). ROC curve analysis showed that the AUC of RDW, NT-proBNP alone and combined for prediction of AKI after AMI were 0.7,0.788 and 0.871, respectively. Conclusions The increase of RDW and NT-proBNP is closely related to the occurrence of AKI after AMI. The combined detection of RDW and NT-proBNP has high predictive value for the occurrence of AKI in patients with AMI.

Abstract:Myocardial infarction (MI) and its concomitant malignant arrhythmia, pathological ventricular remodeling and other complications are seriously harmful to human health. At present, drug therapy is the main strategy to stabilize plaque and reduce myocardial ischemia-reperfusion injury. Recent studies have shown that nano-drug delivery has great potential to benefit targeted therapy and enhance the safety and efficacy of drug treatment. This paper summarizes the present development of nano-drug delivery, and reviews the prospects of the treatment of myocardial infarction and its complications.

Abstract:Wnt signaling pathway regulates a variety of biological behaviors during embryonic development, including cell proliferation, apoptosis, cell polarity and organogenesis, and plays an important role in embryonic development.In an adult, it is thought to be silent. However, recent evidences show that Wnt signaling is reactivated in many biological processes and disease. It is involved in metabolism, inflammation, tumor and other diseases. Meanwhile, the signaling pathway regulates bone homeostasis, promotes osteoblast differentiation, induces bone formation, and is closely related to the development of atherosclerosis and vascular calcification. This review focuses on the effects of continuous activation of this signaling in endothelial dysfunction, inflammation, smooth muscle cell proliferation, and promotion of atherosclerosis and vascular calcification.

Abstract:Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a member of the proteinase K subfamily of the proprotein convertase family, which can combine with low-density lipoprotein receptor (LDLR), and inhibit the repeated use of LDLR, resulting in a decrease in LDLR on the surface of liver cells, an increase in LDL levels in peripheral blood and a series of pathophysiological processes such as abnormal blood lipid metabolism. Current studies have shown that PCSK9 has a certain correlation with myocardial infarction, and may regulate the occurrence and development of myocardial infarction through a way independent of low-density lipoprotein cholesterol (LDLC). This article will review the research progress of PCSK9 and myocardial infarction.

Abstract:MicroRNAs (miRNAs), a large class of short non-coding RNAs, can directly bind to the 3′ untranslated region of target genes, thus affecting gene expression and playing a key role in cardiovascular diseases. Among them, miRNA-206 (miR-206) is a key regulator of heart development and physiological activities, and can not only be used as a marker molecule for diagnosis, but also as a targeted action point for disease treatment. This paper reviews the basic functions of miR-206 in regulating cardiomyocytes, endothelial cells, smooth muscle cells, autonomic nerve cells and other cells, as well as the specific roles and mechanisms of miR-206 in the occurrence and development of coronary artery disease, myocardial infarction, heart failure, arrhythmia, pulmonary hypertension and other diseases.