Abstract:Atherosclerosis (As) is the most common lesion of cardio-cerebrovascular disease endangering human health in the modern society. Finding the potential biomarkers during the progress of As is significant for the prevention and treatment of As-related diseases. Studies have shown that long non-coding RNA (lncRNA) can be widely involved in many cell activity regulation processes, and play a role in different stages of As development. LncRNA can be secreted into the circulatory system by exosome, micro-vesicle and apoptotic bodies. In the recent years, investigations on the circulating lncRNA in As have been reported more and more. The circulating lncRNA is expected to become the novel non-invasive biomarker to monitor the progress of As.

Abstract:Aim To investigate the effects and mechanisms of nuciferine (NF) on the expression of ATP binding cassette transporter A1 (ABCA1) and cholesterol efflux in THP-1 macrophages-derived foam cells. Methods THP-1 cells were differentiated into macrophages by 160 nmol/L phorbol myristate acetate. THP-1 derived macrophages were incubated with 50 mg/L oxidized low density lipoprotein to induce foam cells and cultured with typical approaches. Lipids contents were tested with high performance liquid chromatogram. Liquid scintillation counter was used to determine the efficiency of cholesterol efflux. Real-time PCR and Western blot were used to quantify the expression of ABCA1. The THP-1 macrophages derived foam cells were pretreated with peroxisome proliferator-activated receptor γ (PPARγ) inhibitor GW9662 or LXRα inhibitor GGPP to detect the expression of ABCA1 by real-time quantitative PCR and Western blot. Results NF obviously reduced the intracellular Lipids contents, increased the ABCA1 expression and cholesterol efflux in THP-1 macrophages derived foam cells. PPARγ inhibitor GW9662 and LXRα inhibitor GGPP both interfered NF-promoted ABCA1 expression. Conclusion NF up-regulates the expression of ABCA1 by PPARγ/LXRα pathway to promote the cholesterol efflux and reduce the lipid accumulation in THP-1 macrophages derived foam cells.

Abstract:Aim To explore the role of gap junctions on the regulation of vascular tension and the repair of vascular injury. Methods Vascular rings from rat carotid artery were made and used to compare to the changes of vascular response to norepinephrine (NE) or acetylcholine (Ach) with or without 18α-GA. The model of vascular injury was established with rat carotid balloon injury. And animals were administrated with intraperitoneal injections of carbenoxolone (3 mg/(kg·d)) in carbenoxolone group or saline (2 mL/d) in control group for 2 weeks after carotid balloon injury. After 2 weeks, HE staining and DAPI-Evens blue double staining were applied to evaluate the neointimal formation of targeted vessels. And cell immunofluorescence staining and Western blot were used to detect connexin 43 (Cx43) expression on targeted vessels. Results 18α-GA alone didn’t cause significant response of vascular rings to systole or diastole. In control group, NE or Ach could induce vascular rings to contract or relax, but 18α-GA could inhibit the contraction or relaxation of vascular rings triggered by NE or Ach (NE:0.60±0.03 vs. 0.21±0.04; Ach:0.15±0.01 vs. 0.62±0.03; P＜0.05). 2 weeks after carotid balloon injury, carbenoxolone could significantly reduce the neointimal formation and the stenosis of blood vessel lumen. The number of neointimal nuclei in the carbenoxolone group was significantly lower than that in the control group (89±28 vs. 236±15, n＝5, P＜0.01). Immunofluorescence staining showed that Cx43 was abundant in neointima. Western blot results also suggested that the expression of Cx43 in the carbenoxolone group was significantly lower than that in the control group (0.93±0.06 vs. 0.38±0.11, n＝3, P＜0.01). Conclusions Gap junctions participate in maintaining and regulating vascular tension under the physiological condition, and promote the neointimal formation after vascular injury under the pathological condition. Hence, gap junctions play a key role on the development and progression of vascular injury diseases.

Abstract:Aim To investigate the effect of serum amyloid P component (SAP) on the formation and development of foam cells by observing the formation of foam cells, the morphology of lipid droplets and the expression of lipid droplet surface protein molecules. Methods THP-1 cells were induced to differentiate into macrophages after 48 hours of PMA treatment, and then foam cells were induced by oxidized low density lipoprotein (ox-LDL) combined with lipopolysaccharide (LPS) as control group. Different concentrations of SAP (0,0 mg/L) were added to the experimental group for intervention. Oil red O staining was used to analyze the effect of SAP on foam cell formation and lipid accumulation, and Bodipy493/503 staining was used to observe the morphology and quantity of lipid droplets in foam cells under fluorescence microscope. The lipids in the foam cells were extracted and the contents of triglyceride (TG) and cholesterol ester (CE) in the foam cells were quantitatively determined by kit. Western blot was used to analyze lipid droplet surface related proteins, such as acetyl coenzyme A carboxylase (ACC1), adipogenesis related protein (ADRP), 47 kDa telopenin (TIP47), histone demethylase (JMJD3), fatty acid synthase (FAS). Results Oil red O staining and Bodipy493/503 staining showed that intracellular lipid droplets in the experimental group were larger and more numerous, and the trend was more obvious in the 20 mg/L SAP intervention group than in the 10 mg/L SAP intervention group. The results showed that SAP could enhance the expression levels of ADRP, TIP47, JMJD3 and FAS. Except for the same expression level of FAS in different concentration of SAP intervention group, the expression level of FAS increased with the increase of SAP concentration. Conclusion SAP can promote the formation of foam cells and enhance the accumulation of lipid, SAP can enhance the expression of related lipoproteins.

Abstract:Aim To study the regulatory effect of apolipoprotein(a) (Apo(a)) expression in HepG2 cells by maternal gene 3 (MEG3) and its mechanism. Methods The targeted binding of MEG3 to miR-125a-5p was analyzed using the luciferase reporter enzyme system. Real-time quantitative PCR (qRT-PCR) was used to detect the expression of MEG3 in HepG2 cells with high expression of Apo(a) and SMMC7721 cells with low expression of Apo(a); MEG3 was transfected into HepG2 cells, and expression of Apo(a) and TET2 were detected by Western blot and qRT-PCR. TET2 expression was silenced using small interfering RNA technology. Results MEG3 and hsa-miR-125a-5p could complement each other. Systematic analysis of luciferase reporter gene confirmed the presence of MEG3 binding to hsa-miR-125a-5p. miRNA microarray results showed that the expression level of hsa-miR-125a-5p increased in HepG2 cells, which was nearly 1.5 times higher than that in the control group. Both HepG2 cells and SMMC7721 cells expression MEG3, but the expression level of MEG3 in HepG2 cells is significantly lower than SMMC7721. MEG3 transfection inhibited Apo(a) expression. Mechanism study found that, MEG3 downregulated the expression of miR-125a-5p and upregulated TET2 expression; miR-125a-5p mimics reversed the effect of MEG3, but can be reversed by inhibitors of miR-125a-5p; TET2 silencing can reverse the downregulation Apo(a) expression effect of MEG3. Conclusion MEG3 downregulates the expression of Apo(a) in HepG2 cell through miR-125a-5p/TET2 pathway.

Abstract:Aim To explore the regulating effect of Shengmaisan on insulin resistance and inflammation factors in rat with type 2 diabetes. Methods The Sprague Dawley rats were induced by feeding high fat diet after injection with Santa Terezinha (STZ) in order to copy the model and then they were randomly divided into six groups, the normal control group, the model control group, the Aspirin group and the low-dose, middle-dose and high-dose of Shengmaisan treatment groups. The low-dose, middle-dose and high-dose of Shengmaisan treatment groups were respectively given 4.7 g/(kg·d),9.4 g/(kg·d) and 18.8 g/(kg·d) of Shengmaisan decoction by gavage. Aspirin group was given 0.2 g/(kg·d) of aspirin suspension by gavage. The model control group and normal control group were given equivalent dose of normal saline by gavage. After four weeks administration, the fasting blood-glucose(FBG),fasting insulin(FINS),insulin sensitivity index(ISI) and homeostasis model assessment-estimated insulin resistance(HOMA-IR) were observed, and the content of serum tumor necrosis factor-α (TNF-α ), plasminogen activator inhibitor-1(PAI-1), interleukin-6(IL-6), C-reaction protein (CRP) were assayed by ELISA. Results After four weeks of medication, levels of FBG,FINS and HOMA-IR were remarkably decreased and ISI were remarkably increased in middle-dose treatment group, high-dose treatment group and aspirin group compared with the model control group (P＜0.05); Compared with aspirin group, levels of FBG,FINS,HOMA-IR were increased in low-dose treatment group, while remarkably decreased in middle-dose treatment group and high-dose treatment group; levels of ISI were decreased in low-dose treatment group, while remarkably increased in middle-dose treatment group and high-dose treatment group (P＜0.05); Compared with model control group, the content of serum TNF-α, PAI-1, IL-6, CRP were significantly lower in low-dose, middle-dose and high-dose treatment groups and aspirin group (P＜0.05). Conclusion Shengmaisan has certain protective effects on improving insulin resistance in type 2 diabetic rats by a mechanism that may be associated with the inhibition of inflammatory factors release.

Abstract:Aim To investigate the association between serum bone morphogenetic protein-2 (BMP-2), bone morphogenetic protein-4 (BMP-4) levels and the severity of vascular calcification in CKD rat model. Methods Fifty-five SD rats were randomly divided into control group (n＝20) and CKD group (n＝35). The rats were sacrificed at 2,4, 6,8 week respectively. The kidney and aortic pathologies were analyzed. Blood biochemical indicators, serum BMP-2 and BMP-4 levels, and aortic calcium content were determined. The expression levels of BMP-2, BMP-4 were examined by immunohistochemistry. Results Compared with control group, the CKD rats exhibited a significantly increase in 24 h urinary protein, serum urea nitrogen, creatinine and cystatin C (P＜0.05). Kidney HE staining showed that renal tubular expansion began to emerge since the second week, accompanying with brown yellow substance deposition, interstitial fibrosis, glomerular partial atrophy, and inflammatory cells infiltration. Alizarin red staining showed massive granular deposition and formation of calcified nodules in aorta at the 8th week. The aortic calcium content was significantly increased, which was positively correlated with serum BMP-2 (r＝0.929, P＜0.01) and serum BMP-4 (r＝0.702, P＜0.01) levels in CKD rats. The expression of BMP-2 and BMP-4 in aorta increased significantly after successful establishment of the model at the fourth week. Conclusion Elevated serum BMP-2 and BMP-4 levels may serve as serum markers for CKD vascular calcification.

Abstract:Aim Investigate whether the Geriatric Nutritional Risk Index (GNRI), a combined nutritional score based on serum albumin levels and the body mass index (BMI), was associated with mortality in patients with acute ST-segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI). Methods 309 consecutive patients with STEMI undergoing PCI were prospectively enrolled. Results Patients were then divided into two groups according to GNRI ROC:GNRI≥94 or GNRI＜94 were assigned a GNRI score of 0 or 1, respectively. Of the 309 STEMI patients, 24 (7.74%) died in the hospital, and 15 (4.83%) died during long-term follow-up (median follow-up time, 19.5(3～36) months). Compared with patients with a GNRI of 0, patients with a GNRI of 1 had significantly higher in-hospital (16.7% vs 4.4%; P<0.001) and long-term follow-up (23.8% vs 8.4%, P<0.001) mortality rates. GNRI(HR 2.9,5%CI 1.038 to 4.004, P=0.039) was a significant independent predictor of mortality in patients with STEMI undergoing PCI. Moreover, cumulative survival was significantly lower for patients with a GNRI of 1 compared with patients with a GNRI of 0 (76.2% vs 91.6%, log-rank P<0.001). Conclusion GNRI appears useful for the risk stratification of STEMI patients undergoing PCI.

Abstract:Aim To investigate the incidence, clinical characteristics and risk factors of intraprocedural thrombotic events (IPTE) during percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI) and analyse the influences of IPTE on heart function and major adverse cardiac events (MACE). Methods From January 2013 to December 2014, a total of 836 consecutive AMI patients from Hainan General Hospital who underwent PCI were enrolled in this study (708 male, aged 61.05±11.96 years; 128 female, aged 68.18±10.42 years). The patients with thrombotic events occurred during PCI were enrolled in IPTE group. The patients without thrombotic events were enrolled in non intraprocedural thrombotic events (NIPTE) group. Blood routine test, biochemical test and coagulation test were obtained before PCI. Risk stratification were noted by the GRACE scores, CURSADE scores, SYNTAX scores and thrombus burden scores. Independent sample t test, multiple Logistic regression analysis and other testing methods were applied. Results IPTE occurred in 166 cases (19.86%) during PCI, 670 cases were enrolled in NIPTE group. There was no significant difference between the two groups in SYNTAX scores. Thrombus burden scores were higher in IPTE group than those in NIPTE group (1.11±0.78 vs. 0.57±0.70, P＜0.001). The level of admission CK-MB (127.20±138.36 U/L vs. 89.67±139.25 U/L, P＜0.01), admission TNT (2.30±3.04 μg/L vs. 1.81±2.59 μg/L, P＜0.05), hs-CRP (28.90±43.97 mg/L vs. 22.96±30.92 mg/L, P＜0.05), counts of white blood cell (11.50±3.94 10⁹/L vs. 10.43±3.63 10⁹/L, P＝0.001) and Hcy (17.26±15.28 μmol/L vs. 14.41±8.33 μmol/L, P＜0.05) were higher in IPTE group than those in NIPTE group. The incidence of heart failure was higher in IPTE group than that in NIPTE group (30.1% vs. 22.2%, P＜0.05). There were no significant difference of cardiovascular death, reinfarction, cardiac shock, sudden death and MACE between the two groups. Multiple Logistic regression analysis showed age (OR＝1.9,5%CI was 1.017～1.062, P＜0.001), GLU (OR＝1.7,5%CI was 1.023～1.197, P＜0.05), reduced FIB (OR＝0.8,5%CI was 0.644～0.893, P＜0.05), shortened TT (OR＝0.4,5%CI was 0.990～0.998, P＜0.01), Hcy (OR＝1.3,5%CI was 1.010～1.058, P＜0.01), RBC (OR＝2.8,5%CI was 1.357～3.183, P＜0.01) and thrombus burden scores (OR＝2.3,5%CI was 2.067～3.719, P＜0.001) were independent risk factors associated with IPTE. ConclusionsThe incidence of IPTE during PCI in AMI patients was 19.86% in our study. The patients with IPTE presented higher incidence of heart failure. Age, GLU, FIB, TT, Hcy, RBC and thrombus burden scores were independent risk factors associated with IPTE.

Abstract:Aim To study the characteristics of aspirin and clopidogrel pharmacogenomic testing results in Chinese patients, and to evaluate the clinical application using this technology as an individualized medication guidance after coronary artery bypass grafting. Methods Eight hundred fourty six patients who underwent coronary artery bypass grafting were included. All patients underwent preoperative aspirin and clopidogrel gene detection. The characteristics of the two drugs' testing results were counted respectively. Postoperative individualized antiplatelet therapy was implemented according to the genetic testing results and the evidence-based suggestions. The postoperative inpatients' arterial thrombosis events and the hemorrhage rate associated with antiplatelet drugs application were analyzed. The thrombelastogram (TEG) was used to verify the antiplatelet efficacy randomly. Results The platelet endothelial aggregation receptor 1 (PEAR1) gene was detected for patients with aspirin medication, including 321 cases of wild type (GG) (37.9%), 407 cases of heterozygous mutation (GA) (48.1%), and 118 cases of homozygous mutation (AA) (14%). The aluminium,magnesium and aspinin tablets (Ⅱ) (114 mg/ day) for antiplatelet therapy was applied for the wild type patients over 70 years old, or with a history of peptic ulcer or subtotal gastrectomy. For the remaining patients, aspirin enteric-coated tablets with routine dose (100 mg/ day) was used. Clopidogrel's detected genes were CYP2C19 and PON1. The genotype combination of GG+GG, GG+GA and GA+GG indicates a good response to clopidogrel or a low risk of resistance. Such patients, a total of 429 cases (50.7%), were given a conventional dose of clopidogrel (75 mg/day). On the contrary, genotype combination of AA+AA, AA+GA, AA+GG, GA+AA, GA+GA and GG+AA indicates a high risk of clopidogrel genetic resistance. For these patients, a total of 417 cases (49.3%), the dose of clopidogrel for antiplatelet therapy should increase at least by 50%～70%. Ticagrelor 180 mg/day (two doses) was used for those that were not suitable. In the postoperative hospital-stay period, there were 4 cases of myocardial infarction, 3 cases of cerebral infarction, and 3 cases of bleeding associated with antiplatelet drugs (2 cases of epistaxis and 1 case of gingival bleeding). There were 109 cases received the platelet function test of TEG on 3～5 days after oral antiplatelet therapy randomly. The inhibition rate of AA was (63.48±8.85)%; the inhibition rate of ADP was (53.43±14.10)%; and the MAADP value was 36.67±6.25 mm.Conclusions For the dual antiplatelet therapy after coronary artery bypass grafting, single center results showed that Chinese people had high probability of clopidogrel gene resistance. Gene detection technology has important reference value in the selection of clopidogrel and ticagrelor. For patients with high risk factors for gastrointestinal bleeding, the results of aspirin gene detection can be used as an important basis for drug reduction.

Abstract:Aim To establish the multiple risk factors models for patients with coronary heart disease(CHD) of different genders and then quantitatively analyze the risk of all factors. Methods A total of 8028 CHD inpatients and a control group of 336 cases without significant coronary artery stenosis were enrolled consecutively from January 2009 to January 2018. And they were divided into 4 groups of female CHD (n=2894), male CHD (n=5134), female control(n=129) and male control (n=207). All demographic and clinical data were collected by the physicians and master degree candidates in the division of cardiology. Results The Logistic regression models of multiple risk factors were established for CHD by different genders. More than 55 years of age, dyslipidemia, type 2 diabetes mellitus and hypertension were all independent risk factors of CHD for different genders(P＜0.05). However, the same risk factor had dramatically different pathogenic effects on CHD in male and female. The odds ratio (OR) was markedly different for females and males patients, per 10-year increased over 55 years old (2.597 vs 1.424), dyslipidemia(3.297 vs 1.398), hypertension(1.484 vs. 1.800), type 2 diabetes mellitus(3.187 vs 2.303), respectively(all P＜0.05). In addition, the family history of CHD increased the risk of CHD attack in females by 3.714 times (P＜0.05). Comparatively speaking,the history of smoking increased the risk of CHD attack in males by 5.642 times (P＜0.05). Conclusions Dyslipidemia and type 2 diabetes mellitus may present higher risk of CHD attack in females than males. However, history of smoking and hypertension are much more dangerous for males with CHD.

Abstract:Aim To study the effect of low T3 syndrome on the prognosis of patients with acute myocardial infarction undergoing percutaneous coronary intervention (PCI). Methods From January 1,0 to October 1,4, 1604 patients with acute myocardial infarction diagnosed in the Department of Cardiology of Shengjing Hospital were enrolled in this study. They were divided into two groups according to whether they were complicated with low T3 syndrome:low T3 syndrome group (n=107) and normal thyroid function group (n=1497). Their general date, coronary angiographic data, PCI data, postoperative medication, and end-point events were recorded. The clinical characteristics and prognosis of the two groups were analyzed retrospectively. Results During the follow-up period, there were significant differences in all-cause mortality and cardiac mortality between the two groups (P＜0.05). COX analysis showed that low T3 syndrome was independently associated with all-cause mortality (HR＝2.7,5%CI was 1.039～4.393, P＝0.039) and cardiac death (HR＝2.6,5%CI was 1.379～5.669, P＝0.004). Conclusion Patients with acute myocardial infarction combined with low T3 syndrome undergoing PCI had worse prognosis.

Abstract:Aim To investigate the relationship between nonalcoholic fatty liver disease (NAFLD) and contrast-induced nephropathy (CIN) in patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI). Methods A total of 261 consecutive patients with acute myocardial infarction undergoing PCI in our hospital from March 2014 to May 2016 were enrolled in this study. Patients were divided into NAFLD group (n＝117) and non-NAFLD group (n＝144) based on the diagnosis of B-mode ultrasound. CIN was defined as≥44.2 μmol/L or ≥25％ increase from baseline serum creatinine within 48～72 hours after contrast medium exposure, and that was not attributable to other causes. The following data were recorded:the baseline measurements, blood urea nitrogen, serum creatinine levels before PCI and 1,2 and 3 days after PCI, estimated glomerular filtration rate (eGFR), the contrast volume and coronary pathological features after PCI. Risk factors for CIN were determined by multivariate Logistic regression analysis. Results CIN occurred in 16.5% (43/261) of patients, and incidence of CIN was significantly higher in the NAFLD group than that in the non-NAFLD group [23.93%(28/117) vs. 10.42% (15/144), P＝0.003]. Compared with adverse events in the hospital, the incidence of acute heart failure in NAFLD group was higher (P＜0.05). Multivariate Logistic regressive analysis showed that NAFLD (OR＝2.18), diabetes (OR＝2.42), contrast volume (OR＝2.44) were risk factors for the incidence of CIN. Conclusion NAFLD is the independent risk predictor of CIN in patients with AMI undergoing PCI.

Abstract:Aim To explore the effect of complete revascularization (CR) on long-term prognosis in elderly patients with acute non-ST-segment elevation myocardial infarction (NSTEMI) complicated with multivessel disease (MVD).Methods According to the management of coronary artery, 603 consecutive elderly patients with acute NSTEMI and MVD were divided into two groups:single culprit revascularization (SR) group (n＝260) and complete revascularization (CR) group (n＝343). The endpoints were set as all-cause death, cardiovascular death, nonfatal reinfarction and unplanned repeat revascularization at one year after percutaneous coronary intervention (PCI) surgery. The effects of CR on long-term prognosis in elderly patients with acute NSTEMI combined with MVD were analyzed by COX regression analysis. Results Compared with SR group, the ratio of previous PCI treatment was lower, ratio of triple-vessel disease and preoperative TIMI 0 or 1 were higher, the number and length of implanted stents were also more and longer, proportion of tiglilol use was higher while proportion of nitrates was lower, in CR group. During the follow-up period, the overall all-cause mortality was 4.8% (SR group vs CR group was 6.2% vs 3.8%, P＝0.179), cardiac mortality was 4.1% (SR group vs CR group was 4.6% vs 3.8%,P＝0.615), rate of nonfatal reinfarction was 2.5% (SR group vs CR group was 1.2% vs 3.5%,P＝0.067), rate of unplanned repeat revascularization was 6.8% (SR group vs CR group was 9.6% vs 4.7%,P＝0.017). The single factor COX regression analysis showed that CR significantly reduced the rate of unplanned repeat revascularization in elderly NSTEMI patients with MVD (HR 0.1,5%CI 0.251-0.882, P＝0.019). After correcting the various clinical factors, the multi-factor COX regression analysis also got the same conclusion (HR 0.8,5%CI 0.229-0.837, P＝0.012). However, no matter single factor analysis or multiple factors analysis, CR had no significant effect on all-cause death, cardiac death and nonfatal reinfarction in elderly NSTEMI patients with MVD. In terms of perioperative complications, there was no significant difference in the incidences of BARC grade 3 or 5 bleeding, contrast-induced nephropathy, stroke and acute stent thrombosis between the two groups. Conclusion CR can significantly reduce the rate of unplanned repeat revascularization in elderly patients with NSTEMI and MVD, and it is also safe during perioperative period.

Abstract:Atherosclerosis (As) is associated with iron metabolism. It is still controversial whether the iron gathered in plaque is a pathogenic factor or a simple consequence caused by hemolysis in the development of As disease. Macrophages play a key role in the formation and development of As plaques. This review summarizes the research progress of macrophage iron metabolism and As. This paper first introduces the Hepcidin-Fpn1 axis that plays an important role in macrophage iron metabolism, and then introduces the effect of macrophage iron metabolism on the development of As from 3 aspects of inflammation, infection and hemorrhage in plaque. Finally, the new ideas of As therapy related to iron metabolism are introduced.

Abstract:As an important risk factor for the development of atherosclerosis, the occurrence of obesity is accompanied by changes in cholesterol content and distribution in adipocytes. Cholesterol is an essential component and regulator of lipid rafts in cell membrane. Moreover, it itself is a signaling molecule, which can directly regulate the metabolism and function of adipocytes. The ability of adipocytes to synthesize cholesterol is very limited, so they rely mainly on uptake and flow to regulate cholesterol homeostasis. Recent studies have found that blocking the active efflux of cholesterol on fat cells can inhibit the occurrence of obesity. This article will detailedly describe the cholesterol uptake and efflux pathways of adipocytes, and elucidate the importance of cholesterol homeostasis for adipocytes and the role of adipocyte cholesterol homeostasis in the development of atherosclerosis.

Abstract:Myocardial ischemia reperfusion injury is a pathophysiological process that causes damage to myocardial structure and dysfunction, and further development leads to multi-organ dysfunction of cascade. Mitochondria is an organelle that is complex in structure and responsive to external environment, and its steady state depends on the relative stability of normal form, function and quantity. Mitochondrial quality and metabolic abnormalities are closely related to the occurrence of cardiovascular diseases, especially myocardial ischemia reperfusion injury. MicroRNAs are the regulatory factors that have important role in myocardial mitochondrial protection during ischemia reperfusion injury in recent years. In this paper, the regulation mechanism of mitochondrial morphology, function, mitochondrial autophagy and mitochondrial DNA by microRNAs were reviewed. It provides a theoretical basis for the follow-up study of microRNA in ischemia reperfusion myocardial mitochondrial injury.

Abstract:Atherosclerosis is a common cardiovascular metabolic disease, and its main complications, myocardial infarction and ischemic stroke, have become the first cause of death in the world. The formation of foam cells plays a key role in the development and progression of atherosclerosis. The production of these cells is closely related to intracellular lipid accumulation. Adipose differentiation-related protein (PLIN2) can promote intracellular lipid accumulation. This article mainly discusses the effect of PLIN2 on lipid accumulation in the formation of foam cells, providing new ideas for the prevention and treatment of atherosclerosis.