Cardiovascular Therapeutics最新文献

{"title":"Beta-Blockers for Primary Prevention of Anthracycline-Induced Cardiac Toxicity: An Updated Meta-Analysis of Randomized Clinical Trials","authors":"Armin Attar,&nbsp;Arman Karimi Behnagh,&nbsp;Mehrasa Hosseini,&nbsp;Foad Amanollahi,&nbsp;Paria Shafiekhani,&nbsp;Ali Kabir","doi":"10.1155/2022/8367444","DOIUrl":"10.1155/2022/8367444","url":null,"abstract":"<div>\u0000 <p><i>Aim</i>. Cardiotoxicity is a well-recognized complication of chemotherapy with Anthracyclines. However, results from trials evaluating beta-blockers for prevention are controversial. Therefore, we performed a meta-analysis to find whether prophylactic administration of beta-blockers can help prevent Anthracyclines-induced cardiotoxicity. <i>Methods</i>. We assessed randomized trials and observational studies where a prophylactic intervention was compared with a control arm in patients with a normal left ventricular ejection fraction (LVEF) receiving Anthracyclines. The primary outcome was EF reduction. The secondary outcome was the development of Cancer Therapeutics–Related Cardiac Dysfunction (CTRCD), defined as a decrease in the LVEF of &gt;10% to a value of &lt;53%. <i>Results</i>. We included 17 trials comprising 1291 patients (671 patients in the intervention arm and 620 in the control arm). Carvedilol was administered in eight studies, and others used bisoprolol, metoprolol, or nebivolol. Compared with baseline, LVEF reduced in both intervention and control groups after chemotherapy (MD = −1.93<i>%</i>, 95% CI: -2.94, -0.92, <i>p</i> = 0.001, I² = 72.1<i>%</i> vs. MD = −4.78<i>%</i>, 95% CI: -6.51, -3.04, <i>p</i> = 0.001, <i>I</i>² = 91.6<i>%</i>, respectively). LVEF was less reduced among the beta-blocker receivers (MD = 3.44<i>%</i>, 95% CI: 1.41–5.46, <i>p</i> = 0.001, I² = 94.0<i>%</i>). Among the eight studies reporting the incidence of CTRCD, 45 out of 370 participants in the intervention arm and 54 out of 341 in the control arm were reported to experience this complication (RR = 0.76; 95% CI: 0.53,1.09; <i>I</i>² = 24.4<i>%</i>; <i>p</i> = 0.235). <i>Conclusion</i>. Treatment with beta-blockers prevents dilatation of the left ventricle, development of diastolic dysfunction, and reduction of LVEF. However, these hemodynamic effects do not translate into a significant reduction in CTRCD incidence and prevention of hospitalization for heart failure or cardiac death.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9818032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10581157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predicting Risk Factors of Acute Kidney Injury in the First 7 Days after Admission: Analysis of a Group of Critically Ill Patients","authors":"Kexin Wen,&nbsp;Yongqing Huang,&nbsp;Qi Guo,&nbsp;Tao Wu,&nbsp;Juanzhang Liu,&nbsp;Yuping Zheng,&nbsp;Shuxian Zhou,&nbsp;Dengfeng Geng","doi":"10.1155/2022/1407563","DOIUrl":"10.1155/2022/1407563","url":null,"abstract":"<div>\u0000 <p><i>Background</i>. Acute kidney injury (AKI) is a common complication in critically ill patients. Some predictive models have been reported, but the conclusions are controversial. The aim of this study was the formation of nomograms to predict risk factors for AKI in critically ill patients within the first 7 days after admission to the intensive care unit (ICU). <i>Methods</i>. Data were extracted from the Medical Information Mart for Intensive Care- (MIMIC-) III database. The random forest method was used to fill in the missing values, and least absolute shrinkage and selection operator (Lasso) regression analysis was performed to screen for possible risk factors. <i>Results</i>. A total of 561 patients were enrolled. Complication with AKI is significantly associated with a longer length of stay (LOS). For all patients, the predictors contained in the prediction nomogram included hypertension, coronary artery disease (CAD), cardiopulmonary bypass (CPB), coronary artery bypass grafting (CABG), Simplified Acute Physiology Score II (SAPS II), central venous pressure (CVP) measured for the first time after admission, and maximum and minimum mean artery pressure (MAP). The model showed good discrimination (C − index = 0.818, 95% CI: 0.779-0.857). In the subgroup of patients with well-controlled blood glucose levels, the significant predictors included hypertension, CABG, CPB, SAPS II, and maximum and minimum MAP. Good discrimination was also present before (C − index = 0.785, 95% CI: 0.736–0.834) and after adjustment (adjusted C − index = 0.770). <i>Conclusion</i>. Hypertension, CAD, CPB, CABG, SAPS II, CVP measured for the first time after admission, and maximum and minimum MAP were independent risk factors for AKI in critically ill patients.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9797299/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10511180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effect of the Tongyang Huoxue Recipe (TYHX) on the Ito/IKur in Ischemia/Reperfusion Sinoatrial Node Cells","authors":"Yanli Wang,&nbsp;Qiaomin Wu,&nbsp;Jinfeng Liu,&nbsp;Ruxiu Liu","doi":"10.1155/2022/4114817","DOIUrl":"10.1155/2022/4114817","url":null,"abstract":"<div>\u0000 <p><i>Background.</i> The transient outward potassium current (<i>I</i>_to) and the ultrarapid delayed rectifier potassium current (<i>I</i>_Kur) are major potassium currents involved in the repolarization process of sinoatrial node cells (SNCs). <i>Methods and Results.</i> The SNCs of neonatal rats were divided into control, ischemia/reperfusion (I/R), I/R+blank serum, and Tongyang Huoxue recipe (TYHX) serum groups. <i>I</i>_to and <i>I</i>_Kur were recorded using the whole cell patch-clamp technique, and the current-voltage (I-V), steady-state activation (SSA), steady-state inactivation (SSI), and recovery from inactivation (RFI) curves were plotted, respectively. Compared to the control group, both the peak current density and the current density at the voltage of <i>I</i>_to and <i>I</i>_Kur decreased obviously in SNCs after simulated I/R, the SSA curves moved right, and the SSI curves moved left. After TYHX was added to the extracellular solution of SNCs, both the peak current density and the current density at the voltage of <i>I</i>_to and <i>I</i>_Kur increased significantly, the SSA curves moved left, and the SSI curves moved right with a significant difference of <i>V</i>_1/2. The recovery from the <i>I</i>_Kur RFI curves was slightly restored, and the <i>I</i>_to curves did not change. <i>Conclusions.</i> TYHX increases the peak current density, accelerates the activation, and decreases the inactivation of the <i>I</i>_to and <i>I</i>_Kur. This may be the mechanism of TYHX in shortening the action potential duration of repolarization, which accelerates spontaneous pulsation.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9794430/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10501200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vericiguat: A New Hope for Heart Failure Patients","authors":"Raquel Chiles,&nbsp;Rami A. Al-Horani","doi":"10.1155/2022/1554875","DOIUrl":"10.1155/2022/1554875","url":null,"abstract":"<div>\u0000 <p>Heart failure with reduced ejection fraction (HFrEF) is the inability of the heart to adequately contract or eject blood. This heart is unable to produce adequate cardiac output to perfuse vital tissues. At a fundamental level, it is known that the cardioprotective pathway of nitric oxide-soluble guanylate cyclase-cyclic guanosine monophosphate is impaired in heart failure patients. Vericiguat is a novel, orally used, small molecule, and direct stimulator of the soluble guanylate cyclase, and thus, it enhances the production of cyclic guanosine monophosphate. Vericiguat was approved by the FDA in January of 2021 to reduce the risk of cardiovascular death and heart failure hospitalization following a hospitalization for heart failure or need for outpatient IV diuretics, in adults with symptomatic chronic heart failure and ejection fraction less than 45%. In this review, we describe the chemical and mechanistic aspects, pharmacokinetics, adverse effects, and contraindications of vericiguat so as to facilitate its optimal therapeutic use.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9789902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9286293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long Noncoding RNA SNHG4 Attenuates the Injury of Myocardial Infarction via Regulating miR-148b-3p/DUSP1 Axis","authors":"Sheng Wang,&nbsp;Zhaoyun Cheng,&nbsp;Xianjie Chen,&nbsp;Guoqing Lu,&nbsp;Xiliang Zhu,&nbsp;Gaojun Xu","doi":"10.1155/2022/1652315","DOIUrl":"10.1155/2022/1652315","url":null,"abstract":"<div>\u0000 <p><i>Objective</i>. Long noncoding RNAs (lncRNAs), including some members of small nucleolar RNA host gene (SNHG), are important regulators in myocardial injury, while the role of SNHG4 in myocardial infarction (MI) is rarely known. This study is aimed at exploring the regulatory role and mechanisms of SNHG4 on MI. <i>Methods</i>. Cellular and rat models of MI were established. The expression of relating genes was measured by qRT-PCR and/or western blot. <i>In vitro,</i> cell viability was detected by MTT assay, and cell apoptosis was assessed by caspase-3 level, Bax/Bcl-2 expression, and/or flow cytometry. The inflammation was evaluated by TNF-<i>α</i>, IL-1<i>β</i>, and IL-6 levels. The myocardial injury in MI rats was evaluated by echocardiography, TTC/HE/MASSON/TUNEL staining, and immunohistochemistry (Ki67). DLR assay was performed to confirm the target relationships. <i>Results</i>. SNHG4 was downregulated in hypoxia-induced H9c2 cells and MI rats, and its overexpression enhanced cell viability and inhibited cell apoptosis and inflammation both <i>in vitro</i> and <i>in vivo</i>. SNHG4 overexpression also decreased infarct and fibrosis areas, relieved pathological changes, and improved heart function in MI rats. In addition, miR-148b-3p was an action target of SNHG4, and its silencing exhibited consistent results with SNHG4 overexpression <i>in vitro</i>. DUSP1 was a target of miR-148b-3p, which inhibited the apoptosis of hypoxia-induced H9c2 cells. Both miR-148b-3p overexpression and DUSP1 silencing weakened the effects of SNHG4 overexpression on protecting H9c2 cells against hypoxia. <i>Conclusions</i>. Overexpression of SNHG4 relieved MI through regulating miR-148b-3p/DUSP1, providing potential therapeutic targets.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9744614/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10785867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"lncRNA NEAT1 Downregulation Ameliorates the Myocardial Infarction of Mice by Regulating the miR-582-5p/F2RL2 Axis","authors":"Zhenhua Wu,&nbsp;Yunpeng Bai,&nbsp;Yujuan Qi,&nbsp;Chao Chang,&nbsp;Yan Jiao,&nbsp;Yaobang Bai,&nbsp;Zhigang Guo","doi":"10.1155/2022/4481360","DOIUrl":"10.1155/2022/4481360","url":null,"abstract":"<div>\u0000 <p><i>Background</i>. This study is aimed at effectively investigating the role of coagulation factor II thrombin receptor like 2 (F2RL2) in myocardial infarction (MI) as well as the upstream regulatory miRNA and lncRNA. <i>Methods</i>. Regulatory genes of F2RL2 were analyzed using StarBase and verified by dual-luciferase reporter assay. The MI mouse model was established. The left ventricular ejection fraction (EF) and fractional shortening (FS) were examined by echocardiography. The infarct area, pathological changes, and cell apoptosis in mouse myocardial tissue were evaluated using triphenyltetrazolium chloride and Evans blue, hematoxylin-eosin, and TUNEL staining assays. Oxygen-glucose deprivation- (OGD-) induced human cardiac myocytes (HCMs) were cultured and transfected. The cell viability, proliferation, and apoptosis were determined by CCK-8, EdU staining, and flow cytometry assays. The expressions of F2RL2, miR-582-5p, and nuclear paraspeckle assembly transcript 1 (NEAT1) in myocardial tissues and HCMs were quantified by qRT-PCR or Western blot. <i>Results</i>. NEAT1 sponged miR-582-5p which targeted F2RL2. NEAT1 and F2RL2 were highly expressed while miR-582-5p was lowly expressed in MI mice. F2RL2 downregulation prevented the reduction in EF and SF and the elevation in infarct area and cell apoptosis of MI mice. Both F2RL2 and NEAT1 downregulations reversely modulated the decreased viability and proliferation and the increased apoptosis of OGD-induced HCMs, while miR-582-5p inhibitor did oppositely. NEAT1 silencing upregulated miR-582-5p level but downregulated F2RL2 level. miR-582-5p inhibitor upregulated the F2RL2 level. The role of NEAT1 silencing in OGD-induced HCMs was reversed by miR-582-5p inhibitor whose effect was further offset by F2RL2 downregulation. <i>Conclusion</i>. NEAT1 downregulation ameliorates MI by regulating the miR-582-5p/F2RL2 axis, providing novel biomarkers for MI treatment.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9741539/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10414779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Study on Weight Loss Cause as per the Side Effect of Liraglutide","authors":"Jin Yu,&nbsp;Jeongmin Lee,&nbsp;Seung-Hwan Lee,&nbsp;Jae-Hyung Cho,&nbsp;Hun-Sung Kim","doi":"10.1155/2022/5201684","DOIUrl":"10.1155/2022/5201684","url":null,"abstract":"<div>\u0000 <p><i>Purpose</i>. Liraglutide is known to have much lower weight loss effects in real clinical fields than in randomized clinical trials because of its side effects (SE) and discomfort associated with injections. This study is aimed at determining whether the side effects of liraglutide affect weight reduction and its maintenance in real-world practice. <i>Methods</i>. Endocrinologists conducted a retrospective chart review of data from two tertiary university hospitals. All patients who had been prescribed liraglutide at least once between January 2014 and December 2019 were included. For an average of 3 and 6 months, weight changes due to the presence or absence of SE and discontinuation (MAIN or STOP) of liraglutide were checked. <i>Results</i>. Only 40.8% (64/157) of the patients remained on liraglutide for 6 months; 14.7% (23/157) maintained the drug despite SEs (MAIN_SE(+)), and 40.1% (63/157) discontinued the drug despite not having SEs (STOP_SE(-)). At 3 months, there was −5.9 ± 0.6<i>%</i>, −7.9 ± 0.9<i>%</i>, −4.5 ± 0.5<i>%</i>, and −3.4 ± 0.6<i>%</i> weight reduction in the MAIN_SE(-), MAIN_SE(+), STOP_SE(-), and STOP_SE(+) groups, respectively (all <i>p</i> &lt; 0.001 compared to the baseline). However, there were no significant differences in the weight loss between the MAIN (<i>p</i> = 0.062) and STOP (<i>p</i> = 0.204) groups. At 6 months, the weight reduction was −2.0 ± 0.5<i>%</i> (<i>p</i> &lt; 0.001) in MAIN_SE(-), −2.2 ± 0.7<i>%</i> (<i>p</i> &lt; 0.005) in MAIN_SE(+), −1.7 ± 0.7<i>%</i> (<i>p</i> &lt; 0.01) in STOP_SE(-), and −2.0 ± 0.6<i>%</i> (<i>p</i> = 0.01) in STOP_SE(+), compared to baseline. SEs also caused no significant differences in weight loss between the MAIN (<i>p</i> = 0.787) and STOP (<i>p</i> = 0.694) groups. <i>Conclusions</i>. Our study confirmed that the side effects of liraglutide did not affect weight reduction. Moreover, in the real world, the continuous rate of liraglutide use is not high, and the weight gradually increases after 3 months. Therefore, in addition to the side effects of liraglutide, the medical staff should consider various factors that affect drug adherence, consider ways to increase compliance, and continue to ensure management so that patients can maintain their weight.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9733986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10846797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Safety and Efficacy of Bivalirudin versus Unfractionated Heparin Monotherapy in Patients with CAD and DM Undergoing PCI: A Retrospective Observational Study","authors":"Jing Li,&nbsp;Sanbao Chen,&nbsp;Sicong Ma,&nbsp;Mingque Yang,&nbsp;Zizhao Qi,&nbsp;Kun Na,&nbsp;Miaohan Qiu,&nbsp;Yi Li,&nbsp;Yaling Han","doi":"10.1155/2022/5352087","DOIUrl":"10.1155/2022/5352087","url":null,"abstract":"<div>\u0000 <p><i>Introduction.</i> Optimal anticoagulants for patients with diabetes mellitus (DM) undergoing percutaneous coronary intervention (PCI) are unclear. This retrospective observational study is aimed at evaluating efficacy and safety of bivalirudin versus unfractionated heparin (UFH) monotherapy in patients with DM undergoing PCI. <i>Methods.</i> A total of 3890 diabetic patients receiving PCI in the General Hospital of Northern Theater Command were divided into the bivalirudin group (<i>n</i> = 869) and the UFH group (<i>n</i> = 3021) according to different anticoagulant therapy regimens. Indication for PCI was in accordance with current guidelines including national cardiovascular data registry. The primary endpoint was 30-day net adverse clinical events (NACEs). The secondary endpoints included 30-day major adverse cardiac and cerebral events (MACCEs), bleeding events defined according to the Bleeding Academic Research Consortium (BARC) definition, and stent thrombosis (ST). Patients were matched by propensity score at a ratio of 1 : 1. <i>Results.</i> After propensity score matching, the bivalirudin group was associated with a lower incidence of NACEs (3.0% vs. 6.0%, <i>P</i> = 0.003) than the UFH group. The incidence of MACCE (1.7% vs. 3.3%, <i>P</i> = 0.033) was significantly lower in the bivalirudin group, mainly due to a lower mortality rate (0.6% vs. 2.0%, <i>P</i> = 0.010). In addition, patients in the bivalirudin group had less bleeding (1.4% vs. 3.0%, <i>P</i> = 0.022) than those in the UFH group, although BARC 2, 3, and 5 bleeding (0.1% vs. 0.6%, <i>P</i> = 0.218) was numerically lower. <i>Conclusion.</i> In diabetic patients undergoing PCI, bivalirudin was significantly associated with reduced risks of 30-day NACE and MACCE, mainly driven by the lower rates of bleeding and mortality, compared with heparin monotherapy.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9729030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10391557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Noncoding RNA in the Regulation of Acute Aortic Dissection: From Profile to Mechanism","authors":"Ruibin Wei,&nbsp;Yingqing Feng","doi":"10.1155/2022/2371401","DOIUrl":"10.1155/2022/2371401","url":null,"abstract":"<div>\u0000 <p>Aortic dissection is a life-threatening condition caused by a tear in the intimal layer of the aorta or bleeding within the aortic wall, resulting in the separation of the layers of the aortic wall. As Nienaber reported, aortic dissection is most common in people 65–75 years old and has an incidence of 35 cases per 100,000 people per year in this population. Many pathogenic factors are involved in aortic dissection, including hypertension, dyslipidemia, and abnormality of the aortic intima caused by genetic variation. However, with the development of gene sequencing and transgenic technology, genetic methods are being used for the diagnosis and treatment of diseases, including acute aortic dissection. Genetic research on acute aortic dissection began around 2006. Recently, research on acute aortic dissection has mainly focused on microRNA (miRNA). Studies have found that miRNA plays a critical regulatory role in the occurrence and development of acute aortic dissection. By regulating miRNA expression, acute aortic dissection can be prevented and treated.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9699736/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10349159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of lncRNA XIST Ameliorates IL-1β-Induced Apoptosis of HUVECs and Change of Tissue Factor Level via miR-103a-3p/HMGB1 Axis in Deep Venous Thrombosis by Regulating the ROS/NF-κB Signaling Pathway","authors":"Guangxin Cao,&nbsp;Hua Zhou,&nbsp;Dong Wang,&nbsp;Lei Xu","doi":"10.1155/2022/6256384","DOIUrl":"10.1155/2022/6256384","url":null,"abstract":"<div>\u0000 <p><i>Background</i>. The effect of lncRNA X inactive-specific transcript (XIST) inducing cardiovascular diseases on deep vein thrombosis (DVT) and its mechanism has not been reported. In this study, we uncovered the mystery that lncRNA XIST causes DVT with HUVEC dysfunction. <i>Method</i>. The expression levels of lncRNA XIST and miR-103a-3p were detected by qRT-PCR, and HMGB1 expression was determined by qRT-PCR and western blot. The correlations among the expression levels of lncRNA XIST, miR-103a-3p, and HMGB1 were determined by Spearman’s rank-order correlation test. XIST siRNA (si-XIST) was transfected into HUVECs to knock down the intrinsic expression of lncRNA XIST. The influences of si-XIST on interleukin-1 beta- (IL-1<i>β-</i>) treated HUVEC viability and apoptosis and the level of tissue factor (TF) were detected by MTT, flow cytometry, and ELISA kit, respectively. The relationships between lncRNA XIST, miR-103a-3p, and HMGB1 were predicted by the Encyclopedia of RNA Interactomes (ENCORI) database and verified by dual luciferase reporter assay. The effects of lncRNA XIST and miR-103a-3p on HMGB1 expression were detected by qRT-PCR, western blot, and immunofluorescence analysis. The levels of ROS/NF-<i>κ</i>B pathway-related proteins were detected to study the regulatory mechanism of lncRNA XIST/miR-103a-3p/HMGB1 on IL-1<i>β</i>-treated HUVECs apoptosis and change of TF level. <i>Results</i>. The upregulated expression levels of lncRNA XIST and HMGB1 and downregulated level of miR-103a-3p were found in the plasma of DVT patients and IL-1<i>β</i>-treated HUVECs. Si-XIST promoted cell viability and inhibited HUVEC apoptosis and ameliorated the change of TF level triggered by IL-1<i>β</i>. lncRNA XIST sponged miR-103a-3p and miR-103a-3p targeted HMGB1. Si-XIST inhibited the ROS/NF-<i>κ</i>B pathway to suppress HUVEC apoptosis and ameliorate the change of TF level induced by IL-1<i>β</i> via the miR-103a-3p/HMGB1 axis. <i>Conclusion</i>. lncRNA XIST sponged miR-103a-3p improving HMGB1 expression to exacerbate DVT by activating the ROS/NF-<i>κ</i>B signaling pathway. Our findings indicated that lncRNA XIST can be used as a potential therapeutic target in DVT.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9699739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10349161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}