Abstract:Nonalcoholic fatty liver disease, also known as metabolic associated fatty liver disease, is the most common chronic liver disease in the world. Studies have found that nonalcoholic fatty liver disease is associated with an increased risk of cardiovascular disease, and nonalcoholic fatty liver disease itself may be an independent risk factor for cardiovascular disease. In view of the close association between nonalcoholic fatty liver disease and cardiovascular disease, this article reviews the pathophysiological mechanisms linking nonalcoholic fatty liver disease and cardiovascular disease, and provides ideas for the diagnosis and treatment of cardiovascular disease in patients with nonalcoholic fatty liver disease.

Abstract:Aim To observe whether the proliferation and apoptosis of mouse vascular smooth muscle cells(VSMC) were induced by stretch stress (SS) via PKCα phosphorylation and to investigate the role of berberine (BBR) and related mechanism on the process. Methods The experiment was divided into six groups:normal control(NC) group, BBR group, PKCα inhibitor (Go6976) group, SS group, SS+BBR group and SS+Go6976 group. VSMC were pretreated with BBR or Go6976 for 1 h, and stimulated for 15 min with SS at 10% amplitude. PKCα and MAPK (ERK, JNK, p38) phosphorylation were measured by Western blot. After pretreated by BBR or Go6976, and SS stimulation for 1 h, the proliferation (Ki67) and apoptosis (TUNEL) of VSMC were measured by immunofluorescence. Results Compared with the NC group, SS could increase the phosphorylation levels of PKCα and MAPK(ERK, JNK, p38) (P＜0.05), and increase the levels of VSMC proliferation and apoptosis (P＜0.05). BBR could inhibit the phosphorylation levels of PKCα and MAPK (P＜0.05), while inhibiting VSMC proliferation and apoptosis (P＜0.05); Go6976 could inhibit PKCα, ERK and JNK phosphorylation (P＜0.05), but had no effect on the phosphorylation increase of p38, while inhibiting VSMC proliferation and apoptosis (P＜0.05). Conclusion BBR inhibits the phosphorylation of PKCα and MAPK (ERK, JNK, p38) induced by SS, and further inhibits the proliferation and apoptosis of VSMC.

Abstract:Aim To explore the effect and molecular mechanism of procaine on hypoxia induced injury of N9 and PC12 cells. Methods N9 cells and PC12 cells were divided into control group, hypoxia group, low, medium and high dose (hypoxia＋2,6, 18 mg/L procaine) procaine group, anti-miR-con group, anti-miR-369-3p group, miR-con＋high dose procaine group (transfection miR-con＋hypoxia＋18 mg/L procaine), miR-369-3p＋high dose procaine group (transfection miR-369-3p＋hypoxia＋18 mg/L procaine). Flow cytometry was used to detect apoptosis, reagent kit was used to detect the content of reactive oxygen species (ROS) and malondialdehyde (MDA) and the activity of superoxide dismutase (SOD), ELISA was used to detect the levels of inflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). RT-qPCR was used to detect the expression of miR-369-3p. Results Compared with the control group, the apoptosis rate of N9 cells and PC12 cells in the hypoxia group increased, the content of MDA and ROS increased, the activity of SOD decreased, the levels of TNF-α, IL-1β and IL-6 increased, the expression of miR-369-3p increased (P＜0.05). Compared with the hypoxia group, the apoptosis rate of N9 cells and PC12 cells in the low, medium and high dose procaine groups decreased, the content of MDA and ROS decreased, the activity of SOD increased, the levels of TNF-α, IL-1β and IL-6 decreased, the expression of miR-369-3p decreased in a concentration dependent manner (P＜0.05). Compared with the anti-miR-con group, the apoptosis rate of N9 cells and PC12 cells in the anti-miR-369-3p group decreased, the content of ROS and MDA decreased, the activity of SOD increased, the levels of TNF-α, IL-1β and IL-6 decreased (P＜0.05). Compared with miR-con＋high dose procaine group, the apoptosis rate of N9 cells and PC12 cells in miR-369-3p＋high dose procaine group increased, the expression of cleaved Caspase-3 protein increased, the content of MDA and ROS increased, the activity of SOD decreased, the levels of TNF-α, IL-1β and IL-6 increased (P＜0.05). Conclusion Procaine can reduce hypoxia induced injury to N9 and PC12 cells, and its mechanism may be related to inhibiting the expression of miR-369-3p.

Abstract:Aim To investigate the serum level of long non-coding RNA myocardial infarction-associated transcript (lncRNA MIAT) in patients with type 2 diabetes mellitus (T2DM) and coronary heart disease (CHD) and its effect on high glucose (HG)-induced myocardial cell injury. Methods From June 2021 to December 1,0 patients with uncomplicated T2DM who visited Tangshan People's Hospital were regarded as the T2DM group, 100 patients with uncomplicated coronary heart disease (CHD) were regarded as the CHD group, and 100 T2DM patients with CHD were selected as T2DM+CHD group, in addition, 100 healthy people were regarded as the control group. Real-time quantitative PCR (RT-qPCR) was applied to detect the levels of blood MIAT and microRNA-150-5p (miR-150-5p). The human cardiomyocyte line AC16 cells were cultured in vitro and grouped into NG group (5.5 mmol/L normal glucose), HG group (30 mmol/L high glucose), HG+MIAT knockdown negative control (HG+si-NC) group, HG+MIAT knockdown (HG+si-MIAT) group, HG+si-MIAT+miR-150-5p inhibitor negative control (HG+si-MIAT+anti-NC) group, and HG+si-MIAT+miR-150-5p inhibitor (HG+si-MIAT+anti-miR-150-5p) group. RT-qPCR was performed to detect the expression of MIAT and miR-150-5p in cells; MTT assay was performed to detect cell proliferation viability; Flow cytometry was performed to detect apoptosis; ELISA method was implemented to detect lactate dehydrogenase (LDH) content; Western blot was performed to detect protein expressions of cyclin D2 (CCND2),Bü cell-lymphoma-2 gene (Bcl-2), Bcl-2-associated X protein (Bax), and cysteine protease-3 (Caspase-3), cleaved Caspase-3; Dual-luciferase reporter, RNA-binding protein immunoprecipitation (RIP) and RNA pull down were performed to analyze the targeting relationship of miR-150-5p to MIAT and CCND2. Results Compared with control group, CHD group and T2DM group, the expression level of MIAT was obviously increased in T2DM+CHD group by 2.69 times, 1.71 times and 1.42 times (P＜0.05), and the expression of miR-150-5p was obviously decreased by 68.63%, 60.49% and 46.67% (P＜0.05). Correlation analysis showed that the expression level of MIAT were negatively correlated with miR-150-5p in T2DM+CHD patients (r=－0.662, P＜0.001). Compared with NG group, MIAT expression in AC16 cells was increased in HG group by 3.54 times, cell apoptosis rate, LDH activity, Bax protein level, and cleaved Caspase-3/Caspase-3 ratio were increased by 5.22 times, 2.19 times, 2.90 times, and 3.83 times, respectively; The expression of miR-150-5p was decreased by 75.00%, and the proliferative activity of cells at 4,8 and 72 h was decreased by 49.02%, 52.38%, 49.48%, and the protein levels of CCND2 and Bcl-2 were decreased by 72.62% and 78.26%, respectively (all P＜0.05). MIAT knockdown increased the expression of miR-150-5p by 3.46 times, alleviated HG-induced AC16 cell damage and reduced cell apoptosis by 65.73% (all P＜0.05); Inhibition of miR-150-5p significantly weakened the effect of MIAT knockdown on HG-induced AC16 cell damage (P＜0.05). MIAT targeted and negatively regulated miR-150-5p expression, and CCND2 was a target gene of miR-150-5p. Conclusion Serum MIAT level increased in T2DM patients with CHD. MIAT knockdown may antagonize HG-induced human cardiomyocyte injury by regulating miR-150-5p.

Abstract:Aim To investigate the correlation between small dense low density lipoprotein (sdLDL), high sensitivity C-reactive protein (hs-CRP), mean platelet volume/platelet count (MPV/PLT) and the severity of coronary artery lesions in patients with coronary heart disease. Methods From August 2020 to August 1,0 patients with coronary heart disease who were hospitalized in the Department of Cardiology of Shenzhen Third People's Hospital and underwent coronary angiography were selected. According to the results of coronary angiography, they were divided into single-vessel lesion group (n＝50), double-vessel lesion group (n＝50), and multi-vessel lesion group (n＝50). According to clinical classification, they were divided into stable angina pectoris group (SAP group, n＝26), unstable angina pectoris group (UAP group, n＝48), and acute myocardial infarction group (AMI group, n＝76). Serum levels of sdLDL, hs-CRP, and MPV/PLT were measured among various subgroups, and their correlation with the number and clinical classification of coronary artery disease was analyzed. The ROC curve was used to analyze their effectiveness in predicting the severity of coronary artery disease. Results ①The levels of serum sdLDL, hs-CRP and MPV/PLT in the multi-vessel lesion group were 1.2,1.96 and 1.16 times of those in the double-vessel lesion group (all P＜0.05), and 2.8,3.32 and 1.50 times of those in the single-vessel lesion group (all P＜0.05). Serum sdLDL, hs-CRP and MPV/PLT levels in the double-vessel lesion group were 1.7,1.69 and 1.29 times higher than those in the single-vessel lesion group (all P＜0.05). Serum sdLDL and MPV/PLT levels in AMI group were 1.39 and 1.29 times higher than those in UAP group (all P＜0.05), and 1.37 and 1.38 times higher than those in SAP group (all P＜0.05). There were no significant differences in serum sdLDL and MPV/PLT levels between UAP group and SAP group (P＞0.05). The serum hs-CRP level in AMI group and UAP group was 2.59 and 1.85 times of that in SAP group (both P＜0.05), but there was no statistical significance in hs-CRP level between AMI group and UAP group (P＞0.05). ②Ordered Logistic regression analysis showed that increased levels of serum sdLDL, hs-CRP and MPV/PLT were independent risk factors for predicting the severity of coronary heart disease. ③Spearman correlation analysis showed that serum sdLDL, hs-CRP and MPV/PLT levels were not only positively correlated with the number of coronary lesions (correlation coefficients were 0.5,0.569 and 0.495, respectively, P＜0.05), but also positively correlated with clinical classification of coronary heart disease (correlation coefficients were 0.2,0.40 and 0.414, P＜0.05). ④The ROC curve showed that the combined detection of serum sdLDL, hs-CRP and MPV/PLT was more effective in predicting the severity of coronary heart disease than that of a single indicator detection. Conclusion Increased levels of serum sdLDL, hs-CRP and MPV/PLT are independent risk factors for predicting the severity of coronary heart disease, and are positively correlated with the number of coronary artery lesions and clinical classification of coronary heart disease.

Abstract:Aim To investigate the predictive value of serum uric acid levels on the short-term prognosis of patients with ST-segment elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI). Methods 147 STEMI patients in Cangzhou Central Hospital from January 2018 to May 2021 were selected as the study subjects, all patients underwent PCI treatment. Serum uric acid levels were detected 1 h after PCI, followed up for 30 days, and the prognosis was counted, and patients with different prognosis were compared. According to uric acid levels patients were divided into normal uric acid group and hyperuric acid group. The clinical data and the incidence of major adverse cardiovascular events (MACE) were compared between the two groups, the relationship between serum uric acid and disease indicators and prognosis were analyzed, and its predictive prognostic value was evaluated. Results At 30 days follow-up, the incidence of MACE in 147 patients was 27.21% (40/147). Serum uric acid were higher in patients with MACE than those without MACE (P＜0.05); age, Killip classification, Gensini score, proportion without recurrent flow, preoperative and 1 h postoperative serum uric acid levels were higher in the hyperuric acid group than those in the normal uric acid group (P＜0.05); correlation analysis showed that serum uric acid was positively correlated with Killip classification, Syntax score classification, and the incidence of MACE was higher in the hyperuric acid group than that in the normal uric acid group (48.84% vs. 18.27%, P＜0.05). Logistic multivariate analysis showed a significant correlation between serum uric acid and the occurrence of MACE before and after adjusting for other factors such as age, Killip classification, Gensini score, Syntax score classification, no reflow and preoperative serum uric acid levels (P＜0.05). ROC curve analysis showed that the AUC of serum uric acid for predicting MACE was 0.6,5%CI was 0.731～0.901, best cut-off value was 361.37 μmol/L, sensitivity was 70.00% and specificity was 88.79%. Conclusion The serum uric acid level in STEMI patients after PCI is positively correlated with the occurrence of MACE, which can serve as an important indicator for predicting MACE and providing effective information for clinical practice.

Abstract:Aim To explore the association between cardiometabolic index and hyperuricemia risk in people over 45 years of age in China Health and Retirement Longitudinal Study. Methods Data from the China Health and Retirement Longitudinal Study in 2011 and 2015 were included in this prospective cohort study. The 2011 data were used as the baseline and the outcomes of hyperuricemia were followed up in 2015. The Cox proportional hazard model was used to analyze the association between cardiometabolic index and the risk of hyperuricemia. ROC curve was used to analyze the predictive value of cardiometabolic index for the risk of hyperuricemia. Results Among 3 002 subjects, after adjusting for relevant confounders, the risk of hyperuricemia in the highest cardiometabolic index group was 3.12 times (P＜0.001) that in the lowest cardiometabolic index group in males, and HR was 3.0,5%CI was 1.606～6.062; in females was 2.128 times (P＜0.05) that in the lowest cardiometabolic index group, respectively, and HR was 2.8,5%CI was 1.060～4.272; the risk of hyperuricemia increased with the increase of cardiometabolic index. ROC curve analysis showed that the curve of cardiometabolic index for predicting the risk of hyperuricemia was 0.618 (95%CI:0.580~0.656), the best cutoff value was 0.433, the sensitivity was 46.97%, and the specificity was 72.94%. Conclusions The cardiometabolic index is positively correlated with the risk of hyperuricemia. Maintaining a low cardiometabolic index is beneficial to prevent hyperuricemia. It is suggested that cardiometabolic index may be an identification factor of hyperuricemia.

Abstract:Aim To investigate the association between serum remnant cholesterol (RC) level and coronary heart disease (CHD) and myocardial infarction (MI). Methods Two-sample Mendelian randomization (MR) analysis was used to investigate the potential causal association between RC and CHD, MI. The inverse variance weighted (IVW) model was used as the main analytical method for the two-sample MR analysis and was followed by sensitivity analysis, including heterogeneity test, horizontal pleiotropy test, and leave-one-out analysis,to evaluate the robustness of the MR results. Results The IVW method showed statistically significant associations between RC and increased risk of CHD and MI (CHD:OR=1.7,5%CI:1.40～1.76, P＝2.01 E－14; MI:OR=1.9,5%CI:1.40～1.79,P＝1.26E－13). MR-Egger regression results suggested that the screened single nucleotide polymorphisms (SNP) were not genetically pleiotropic with CHD and MI (The P values for CHD and MI were P＝0.924 1 and P＝0.740 5, respectively).Conclusion Elevated serum remnant cholesterol level is causally associated with an increased risk of CHD and MI.

Abstract:Cardiovascular disease is one of the major diseases that seriously threaten the health of Chinese residents, and the fatality rate stands first in the disease spectrum in China for a long term. With the rapid development of population aging, the prevalence and mortality of cardiovascular diseases remain on the rise, and the current treatment effect on and prognosis of heart failure are not satisfactory. It is particularly important to explore the potential pathogenic mechanisms of heart failure and identify new therapeutic targets. This article reviews the research advances in targeted therapy for heart failure in recent years, which may provide new ideas for delaying the progress of heart failure.

Abstract:Ferroptosis is an iron-dependent, non-apoptotic programmed cell death characterized by iron metabolism disorder that leads to intracellular iron overload, which induces lipid peroxidation through fenton reaction and activates ferroptosis. Ferroptosis is associated with many diseases, among which the relationship with abdominal aortic aneurysm has come into attention in the last few years. Abdominal aortic aneurysm is a degenerative disease characterized by structural destruction and irreversible dilation of the abdominal aortic wall. Its pathogenesis is related to oxidative stress, inflammation, loss of vascular smooth muscle cells and vascular calcification. Ferroptosis may play a role in the development of abdominal aortic aneurysm through the above pathways. Therefore, this paper reviews the pathogenesis of ferroptosis and abdominal aortic aneurysm, providing a new idea and target for the abdominal aortic aneurysm treatment.

Abstract:Myocardial infarction with non-obstructive coronary arteries (MINOCA) is a special kind of myocardial infarction, and its prognosis is related to different causes. This review summarized the correlation between inflammation and various causes of MINOCA, and the correlation between inflammatory factors such as C-reactive protein, neutrophil-to-lymphocyte ratio, interleukin-6 and prognosis of MINOCA.

Abstract:Long non-coding RNA (lncRNA) is a class of RNA more than 200 nucleotides long and has no protein-coding capacity, but it plays a very important role in regulating various biological processes such as proliferation, apoptosis, migration, invasion and differentiation. It has found that lncRNA is closely related to the development of myocardial ischemia/reperfusion (I/R) injury. This review discusses the advances in the reduction of myocardial I/R injury and its possible mechanisms by lncRNA.

Abstract:Gout is a common disease caused by the deposition of sodium urate crystals in joints or other tissues, and its incidence and prevalence are increasing year by year. Hyperuricemia is the most important risk factor for gout. In recent years, many epidemiological and empirical studies have confirmed that gout is closely related to the occurrence and death of cardiovascular diseases such as hypertension, coronary heart disease and myocardial infarction. Dual-energy CT, as a new non-invasive imaging modality, can specifically and quantitatively display urate crystals, and has become an effective tool for the diagnosis of gout in recent years, and some studies have found its clinical value in the diagnosis of cardiovascular damage in gout. This review analyzes the complex correlation between gout and cardiovascular diseases, and the advantages and application value of dual-energy CT in the diagnosis of cardiovascular damage in gout.