Cardiovascular Therapeutics最新文献

{"title":"Association between Platelet to Neutrophil Ratio (PNR) and Clinical Outcomes in STEMI Patients after Successful pPCI: A Secondary Analysis Based on a Cohort Study","authors":"Hao Wang, Xiaochun Qing, Hua Wang, Yunfei Gu","doi":"10.1155/2022/2022657","DOIUrl":"https://doi.org/10.1155/2022/2022657","url":null,"abstract":"Purpose This study was aimed at investigating whether the platelet-to-neutrophil ratio (PNR) is independently related to the prognosis of patients with ST-elevation myocardial infarction (STEMI) after successful primary percutaneous coronary intervention (pPCI). Methods This was a secondary analysis of data retrieved from the DATADRYAD database, which was a prospective cohort study. A total of 464 STEMI patients who underwent successful pPCI were recruited between January 2010 and October 2014. The target-independent variable, PNR, was measured at the baseline. The dependent variable in the current study was the occurrence of major adverse cardiovascular events (MACEs) during the 30-month follow-up. Results Two patients were excluded from the final analysis because their platelet counts were unavailable. The average age of the 462 participants was 63 ± 11.92 years, and approximately 76.6% were male. After adjusting for age, sex, anterior wall myocardial infarction (MI), history of MI, apelin-12, apelin-12 change rate, left ventricular end-diastolic diameter, peak cardiac troponin I, pathological Q wave, Killip classification grade, fasting blood glucose, albumin, GENSINI score, and estimated glomerular filtration rate, a nonlinear relationship was found between the PNR and MACEs in the included cohort. The threshold value of the PNR for MACEs was 23.1. Over this cutoff value, the incidence rate of MACEs increased by 43% per 10-unit change in PNR (95% CI: 1.16–1.75, p = 0.0006). Conclusion There was a threshold relationship between PNR and MACEs in patients with STEMI who underwent successful pPCI. The incidence of MACEs was positively associated with the PNR when the PNR exceeded 23.1.","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43676798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CircTRRAP Knockdown Has Cardioprotective Function in Cardiomyocytes via the Signal Regulation of miR-370-3p/PAWR Axis","authors":"Y. Zhang, Zhenggong Li, Jiao Wang, Hao Chen, Rui He, Hongkun Wu","doi":"10.1155/2022/7125602","DOIUrl":"https://doi.org/10.1155/2022/7125602","url":null,"abstract":"Background Circular RNA Transformation/Transcription Domain Associated Protein (circTRRAP, hsa_circ_0081241) was abnormally upregulated in acute myocardial infarction (AMI) patients. However, its biological role and functional mechanism in AMI remain to be researched. Methods Human cardiomyocyte AC16 was exposed to hypoxia to induce cell injury. Cell viability was detected through Cell Counting Kit-8. CircTRRAP, microRNA-370-3p (miR-370-3p), and Pro-Apoptotic WT1 Regulator (PAWR) levels were assayed by reverse transcription-quantitative polymerase chain reaction. Cell proliferation analysis was performed via 5-ethynyl-2′-deoxyuridine (EdU) assay. Cell apoptosis was assessed using flow cytometry and caspase-3 activity assay. The protein levels were measured through western blot. Enzyme-linked immunosorbent assay was used to examine the release of inflammatory cytokines. Oxidative stress was assessed by the commercial kits. Dual-luciferase reporter assay, RNA immunoprecipitation, and RNA pull-down assays were performed for the validation of target interaction. Results CircTRRAP was highly expressed following hypoxia treatment in AC16 cells. Downregulation of circTRRAP promoted cell growth but inhibited apoptosis, inflammation, and oxidative stress in hypoxic cells. CircTRRAP could target miR-370-3p, and the regulatory effects of circTRRAP on the hypoxic cells were associated with the sponge function of miR-370-3p. PAWR served as the target for miR-370-3p, and it was regulated by circTRRAP/miR-370-3p axis. The protective role of miR-370-3p was achieved by downregulating the PAWR expression in hypoxia-treated AC16 cells. Conclusion These findings demonstrated that silence of circTRRAP exerted the protection against the hypoxia-induced damages in cardiomyocytes through regulating the miR-370-3p and PAWR levels.","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44849648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advantages and Disadvantages of Inclisiran: A Small Interfering Ribonucleic Acid Molecule Targeting PCSK9—A Narrative Review","authors":"I. Merćep, Nikolina Friščić, Dominik Strikić, Ž. Reiner","doi":"10.1155/2022/8129513","DOIUrl":"https://doi.org/10.1155/2022/8129513","url":null,"abstract":"As dyslipidemias remain one of the main risk factors for developing cardiovascular disease, the question of maintaining optimal lipid levels with pharmacotherapy remains a subject of interest worldwide. In contrast to conventional pharmacotherapy, human monoclonal antibodies directed against proprotein convertase subtilisin/kexin type 9 (PSCK9) and small interfering RNA- (siRNA-) based drug targeting PCSK9 represent a new strategy for managing lipid disorders and reducing cardiovascular risk. Inclisiran is a long-acting, synthetic siRNA that targets hepatic production of PCSK9 and consequently causes a reduction in LDL-C concentrations by approximately 50% compared to placebo. The structural modification of inclisiran has led to better stability and prolonged biological activity of the drug. The main advantage over conventional pharmacotherapy and anti-PCSK9 monoclonal antibodies is its favorable administration regimen (0–90–180 days), which should lead to much better compliance. Clinical trials conducted so far have confirmed the tolerability and efficacy of inclisiran in long-term PCSK9 and LDL-C level reductions. Moreover, a short-term follow-up on the safety of inclisiran showed a relatively good safety profile of the drug. However, it is still of great importance for ongoing and forthcoming clinical trials to be continued on a larger group of patients in order to assess long-term tolerability, efficacy, and safety of inclisiran.","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44021434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HSPB1 Regulates Autophagy and Apoptosis in Vascular Smooth Muscle Cells in Arteriosclerosis Obliterans.","authors":"Keqin Chen,&nbsp;Changmiao Hou,&nbsp;Lei Xu,&nbsp;Hanwu Peng,&nbsp;Chaogui He,&nbsp;Jing Liu,&nbsp;Guoqing Wang,&nbsp;Shaoshuai Huang,&nbsp;Xiehong Liu","doi":"10.1155/2022/3889419","DOIUrl":"https://doi.org/10.1155/2022/3889419","url":null,"abstract":"<p><strong>Objective: </strong>Small heat shock protein-1 (HSPB1) is a small heat shock protein that participates in many cellular processes and alleviates stress-induced cell injury. Autophagy protects cells from many types of stress and plays a key role in preventing stress in arteriosclerosis obliterans (ASO). However, the roles of HSPB1 in autophagy and apoptosis in the context of ASO pathogenesis remain unclear.</p><p><strong>Methods: </strong>In vivo and in vitro studies were used to determine whether HSPB1 is associated with ASO progression. The expression of HSPB1 was measured in normal and sclerotic blood vessels. The role of HSPB1 and its potential downstream signaling pathway were determined in VSMCs by overexpressing and silencing HSPB1.</p><p><strong>Results: </strong>A total of 91 ASO patients admitted to and treated at our hospital from Sep. 2020 to Sep. 2021 were selected, and plasma HSPB1 expression was assessed. We divided the patients with ASO into the grade I (<i>n</i> = 39), II (<i>n</i> = 29), III (<i>n</i> = 10), and IV (<i>n</i> = 13) groups according to Fontaine's classification. Plasma HSPB1 levels were markedly decreased in patients with grade III (<i>n</i> = 10) and IV (<i>n</i> = 13) ASO compared with patients with grade I ASO. Furthermore, HSPB1 expression was significantly decreased, and p62 and cleaved caspase-3 were increased in the sclerotic vasculature compared to the normal vasculature (<i>p</i> < 0.05). Overexpression of HSPB1 promoted apoptosis of VSMCs following ox-LDL treatment. Knockdown of HSPB1 led to a marked increase in the expression of LC3II and Beclin-1 in ox-LDL-stimulated VSMCs, whereas knockdown of HSPB1 attenuated these changes (<i>p</i> < 0.05). Importantly, overexpression of HSPB1 promoted the dephosphorylation of JNK in ox-LDL-stimulated VSMCs. Conversely, downregulation of HSPB1 induced the opposite change.</p><p><strong>Conclusion: </strong>Loss of HSPB1 promotes VSMC autophagy and inhibits VSMC apoptosis, which are associated with ASO. HSPB1 and its downstream signaling pathways could be potential therapeutic targets for ASO treatment.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 ","pages":"3889419"},"PeriodicalIF":3.1,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9678445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10349163","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 <i>I</i> _to/<i>I</i> _Kur in Ischemia/Reperfusion Sinoatrial Node Cells.","authors":"Yanli Wang,&nbsp;Qiaomin Wu,&nbsp;Jinfeng Liu,&nbsp;Ruxiu Liu","doi":"10.1155/2022/4114817","DOIUrl":"https://doi.org/10.1155/2022/4114817","url":null,"abstract":"<p><strong>Background: </strong>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).</p><p><strong>Methods and results: </strong>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.</p><p><strong>Conclusions: </strong>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>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 ","pages":"4114817"},"PeriodicalIF":3.1,"publicationDate":"2022-01-01","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":"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":"https://doi.org/10.1155/2022/8367444","url":null,"abstract":"<p><strong>Aim: </strong>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.</p><p><strong>Methods: </strong>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 >10% to a value of <53%.</p><p><strong>Results: </strong>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%, 95% CI: -2.94, -0.92, <i>p</i> = 0.001, I² = 72.1% vs. MD = -4.78%, 95% CI: -6.51, -3.04, <i>p</i> = 0.001, <i>I</i> ² = 91.6%, respectively). LVEF was less reduced among the beta-blocker receivers (MD = 3.44%, 95% CI: 1.41-5.46, <i>p</i> = 0.001, I² = 94.0%). 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>p</i> = 0.235).</p><p><strong>Conclusion: </strong>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>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 ","pages":"8367444"},"PeriodicalIF":3.1,"publicationDate":"2022-01-01","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":"https://doi.org/10.1155/2022/1407563","url":null,"abstract":"<p><strong>Background: </strong>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).</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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).</p><p><strong>Conclusion: </strong>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>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 ","pages":"1407563"},"PeriodicalIF":3.1,"publicationDate":"2022-01-01","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":"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":"https://doi.org/10.1155/2022/1652315","url":null,"abstract":"<p><strong>Objective: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>Overexpression of SNHG4 relieved MI through regulating miR-148b-3p/DUSP1, providing potential therapeutic targets.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 ","pages":"1652315"},"PeriodicalIF":3.1,"publicationDate":"2022-01-01","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":"https://doi.org/10.1155/2022/4481360","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>NEAT1 downregulation ameliorates MI by regulating the miR-582-5p/F2RL2 axis, providing novel biomarkers for MI treatment.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 ","pages":"4481360"},"PeriodicalIF":3.1,"publicationDate":"2022-01-01","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":"Inflammatory Response and Immune Regulation in Brain-Heart Interaction after Stroke.","authors":"Lihua Zou,&nbsp;Ruquan Han","doi":"10.1155/2022/2406122","DOIUrl":"https://doi.org/10.1155/2022/2406122","url":null,"abstract":"<p><p>Cerebrocardiac syndrome (CCS) is one of the secondary myocardial injuries after stroke. Cerebrocardiac syndrome may result in a poor prognosis with high mortality. Understanding the mechanism of the brain-heart interaction may be crucial for clinical treatment of pathological changes in CCS. Accumulating evidence suggests that the inflammatory response is involved in the brain-heart interaction after stroke. Systemic inflammatory response syndrome (SIRS) evoked by stroke may injure myocardial cells directly, in which the interplay between inflammatory response, oxidative stress, cardiac sympathetic/parasympathetic dysfunction, and splenic immunoregulation may be also the key pathophysiology factor. This review article summarizes the current understanding of inflammatory response and immune regulation in brain-heart interaction after stroke.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 ","pages":"2406122"},"PeriodicalIF":3.1,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9683992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10349158","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}