Cardiovascular Therapeutics最新文献

{"title":"Liquid Embolization of Peripheral Arteriovenous Malformations with Ethylene-Vinyl Alcohol Copolymer in Neonates and Infants.","authors":"Jochen Pfeifer, Walter A Wohlgemuth, Hashim Abdul-Khaliq","doi":"10.1155/2022/1022729","DOIUrl":"10.1155/2022/1022729","url":null,"abstract":"<p><p>In the postnatal period, extensive peripheral arteriovenous malformations (AVM) are associated with high morbidity, especially when localized in the liver. Their urgent treatment is always a challenging problem in neonates and infants. We analyzed four consecutive children aged three days to three years who underwent eight liquid embolization procedures with ethylene-vinyl alcohol copolymer. The AVM were situated on the thoracic wall, in the liver, and on the lower leg. In three cases, the malformations showed total regression. The tibial AVM degenerated widely. If impaired beforehand, cardiac or hepatic function normalized after the interventions. There were no embolization-associated complications such as nontarget embolization or tissue ischemia. We conclude that application of ethylene-vinyl alcohol copolymer seems to be a safe therapeutic option and can be used in neonates and infants with peripheral AVM in consideration of the agent's characteristics. Nevertheless, there are still hardly any data concerning young children.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2022-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9313932/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40608125","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":"Curcumin Attenuates Ferroptosis-Induced Myocardial Injury in Diabetic Cardiomyopathy through the Nrf2 Pathway.","authors":"Zhang Wei,&nbsp;Qian Shaohuan,&nbsp;Kang Pinfang,&nbsp;Shi Chao","doi":"10.1155/2022/3159717","DOIUrl":"https://doi.org/10.1155/2022/3159717","url":null,"abstract":"<p><p>Diabetes causes lipid peroxide to accumulate within cardiomyocytes. Furthermore, lipid peroxide buildup is a risk factor for ferroptosis. This study is aimed at examining whether curcumin can ameliorate ferroptosis in the treatment of diabetic cardiomyopathy. Hematoxylin and eosin and Masson sections were used to examine the morphology, arrangement, and degree of fibrosis of the myocardium of diabetic rabbit models. The expression levels of nuclear Nrf2, Gpx4, Cox1, and Acsl4 in diabetic animal and cell models were quantitatively analyzed using immunofluorescence and western blotting. Nrf2-overexpression lentivirus vectors were transfected into cardiomyocytes, and the protective effects of curcumin and Nrf2 on cardiomyocytes under high glucose stimulation were assessed using terminal deoxynucleotidyl transferase dUTP nick-end labelling and reactive oxygen species probes. Diabetes was found to disorder myocardial cell arrangement and significantly increase the degree of myocardial fibrosis and collagen expression in myocardial cells. Curcumin treatment can increase nuclear transfer of Nrf2 and the expression of Gpx4 and HO-1, reduce glucose induced myocardial cell damage, and reverse myocardial cell damage caused by the ferroptosis inducer erastin. This study confirmed that curcumin can promote the nuclear translocation of Nrf2, increase the expression of oxidative scavenging factors, such as HO-1, reduce excessive Gpx4 loss, and inhibit glucose-induced ferroptosis in cardiomyocytes. This highlights a potentially new therapeutic route for investigation for the treatment diabetic cardiomyopathy.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2022-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9307414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40572335","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":"Effect of Adiponectin Variant on Lipid Profile and Plasma Adiponectin Levels: A Multicenter Systematic Review and Meta-Analysis.","authors":"Guiqing Wang,&nbsp;Yufeng Wang,&nbsp;Zhi Luo","doi":"10.1155/2022/4395266","DOIUrl":"https://doi.org/10.1155/2022/4395266","url":null,"abstract":"<p><strong>Background: </strong>Adiponectin is a recognized antiatherogenic molecule; this study was aimed at clarifying the effects of adiponectin variants on lipid and adiponectin levels.</p><p><strong>Methods: </strong>By searching PubMed and Cochrane databases for studies published before March 31, 2022, a total of 86,610 individuals were included in the analysis.</p><p><strong>Results: </strong>Variants of rs2241766 and rs266729 were associated with decreased adiponectin and high-density lipoprotein cholesterol (HDL-C), as well as increased triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) levels. In contrast, the rs1501299 variant was correlated with increased adiponectin and HDL-C, as well as decreased TG, TC, and LDL-C levels. Subgroup analysis indicated that the significant effect of the rs2241766 and rs266729 variants on lipid profile was predominant in Chinese, while the significant effect of the rs1501299 variant on lipid profile was primarily in Caucasians. Moreover, a stronger effect of the rs2241766 and rs1501299 variants on LDL-C levels was observed in males, while a considerable effect of the rs266729 variant on LDL-C levels was observed in children.</p><p><strong>Conclusions: </strong>The present study indicated that Chinese with the rs2241766 and rs266729 variants were at high risk of dyslipidemia, atherosclerosis, or coronary artery disease (CAD). Males with the rs2241766 variant were at high risk of CAD. Children with the rs266729 variant had a high risk to develop dyslipidemia, atherosclerosis, and even early onset of CAD in the future. These findings are beneficial to clinical physicians to choose different management strategies for cardiovascular disease (CVD) prevention.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2022-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9283072/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40572336","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":"Retrospective Study of Aging and Sex-Specific Risk Factors of COVID-19 with Hypertension in China.","authors":"Juan Wang,&nbsp;Yili Zhang,&nbsp;Kexin Li,&nbsp;KangJia Du,&nbsp;Xinyi Huang,&nbsp;Zifeng Zhou,&nbsp;Yan Ma,&nbsp;Shuzhen Guo,&nbsp;Yong Hou,&nbsp;Quntang Li,&nbsp;Hongming Xu,&nbsp;Jin Huang,&nbsp;Qiuhua Huang,&nbsp;Hui Na,&nbsp;Jingwei Wang,&nbsp;Xiaoyan Wang,&nbsp;Yanhua Xiao,&nbsp;Junteng Zhu,&nbsp;Hong Chen,&nbsp;Zhang Liu,&nbsp;Mingxuan Wang,&nbsp;Linsong Zhang,&nbsp;Wei Wang,&nbsp;Haitong Wan","doi":"10.1155/2022/5978314","DOIUrl":"https://doi.org/10.1155/2022/5978314","url":null,"abstract":"<p><strong>Background: </strong>Coronavirus disease 2019 (COVID-19) has been a global threat that pushes healthcare to its limits. Hypertension is one of the most common risk factors for cardiovascular complications in COVID-19 and is strongly associated with disease severity and mortality. To date, clinical mechanisms by which hypertension leads to increased risk in COVID-19 are still unclear. Furthermore, additional factors might increase these risks, such as the consideration of age and sex, which are of interest when in search of personalized treatments for hypertensive COVID-19 patients.</p><p><strong>Methods: </strong>We conducted a retrospective cohort study of 543 COVID-19 patients in seven provinces of China to examine the epidemiological and clinical characteristics of COVID-19 in this population and to determine risk factors of hypertensive COVID-19 patients. We also used univariable and multivariable logistic regression methods to explore the risk factors associated with hypertensive COVID-19 patients in different age and sex subgroups.</p><p><strong>Results: </strong>Among the enrolled COVID-19 patients, the median age was 47 years (interquartile range (IQR) 34.0-57.0), and 99 patients (18.23%) were over 60 years old. With regard to comorbidities, 91 patients (16.75%) were diagnosed with hypertension, followed by diabetes, coronary disease, and cerebrovascular disease. Of the hypertensive COVID-19 patients, 51 (56.04%) were male. Multivariable analysis showed that old age, comorbid diabetes or coronary heart disease on admission, increased D-dimer, increased glucose, and decreased lymphocyte count were independent risk factors associated with hypertensive COVID-19 patients. Elevated total bilirubin (odds ratio [OR]: 1.014, 95% confidence interval [CI]: 0.23-1.05; <i>p</i> = 0.043) and triglycerides (OR: 1.173, 95% CI: 0.049-1.617; <i>p</i> = 0.007) were found to be associated with elderly hypertensive COVID-19 patients. In addition, we found that decreased lymphocytes, basophil, high-density lipoprotein, and increased fibrinogen and creatinine were related to a higher risk of disease severity in male patients. The most common abnormal clinical findings pertaining to female hypertensive COVID-19 patients were hemoglobin, total bile acid, total protein, and low-density lipoprotein.</p><p><strong>Conclusions: </strong>Factors associated with increased risk of hypertensive COVID-19 patients were identified. Results to the different age and sex subgroups in our study will allow for better possible personalized care and also provide new insights into specific risk stratification, disease management, and treatment strategies for COVID-19 patients with hypertension in the future.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2022-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9240958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40612938","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":"Inhibitory Effect of <i>Lactobacillus delbrueckii</i> subsp. <i>bulgaricus</i> KSFY07 on Kappa-Carrageenan-Induced Thrombosis in Mice and the Regulation of Oxidative Damage.","authors":"Pan Wang,&nbsp;Fang Tan,&nbsp;Jianfei Mu,&nbsp;Hongjiang Chen,&nbsp;Xin Zhao,&nbsp;Yanan Xu","doi":"10.1155/2022/4415876","DOIUrl":"https://doi.org/10.1155/2022/4415876","url":null,"abstract":"<p><p>A mouse thrombosis model was established by kappa-carrageenan to observe the inhibitory effect of <i>Lactobacillus delbrueckii</i> subsp. <i>bulgaricus</i> KSFY07 (LDSB-KSFY07) on thrombosis and the oxidative stress response. Mouse serum, liver tissue-related indicators, and intestinal microbial composition were measured by examining the expression of microbes in mouse faeces using a biochemical kit, slice observations, and quantitative polymerase chain reaction (qPCR) experiments. The results showed that LDSB-KSFY07 effectively reduced the degree of black tail in thrombotic mice, increased activated partial thromboplastin time (APTT), and decreased thrombin time (TT), fibrinogen (FIB), and prothrombin time (PT) in thrombotic mice. LDSB-KSFY07 was also able to reduce malondialdehyde (MDA) levels and increase superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) levels in the serum and liver tissues of thrombotic mice. Pathological observations showed that LDSB-KSFY07 reduced liver tissue lesions and tail vein thrombosis. Further, experimental results showed that LDSB-KSFY07 was able to upregulate the mRNA expression of copper/zinc-SOD (Cu/Zn-SOD), manganese-SOD, and GSH-Px in the liver tissue of thrombotic mice. Moreover, LDSB-KSFY07 was also able to downregulate the mRNA expression of NF-<i>κ</i>B p65, intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in tail vein vascular tissue. Meanwhile, LDSB-KSFY07 could raise plasminogen activator inhibitor-1 (PAI-1) mRNA expression and reduce tissue plasminogen activator (t-PA) expression in heart and tail vein vascular tissues of thrombotic mice. A mouse faeces examination revealed that LDSB-KSFY07 could also upregulate <i>Bacteroides</i>, <i>Lactobacterium</i>, and <i>Bifidobacterium</i> microbial expression and downregulate <i>Firmicutes</i> expression in the gut. These results indicate that LDSB-KSFY07 was able to inhibit mouse thrombosis and reduce liver oxidative stress damage in thrombus mice and show that high concentrations of LDSB-KSFY07 provided a better response similar to that of the drug heparin.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2022-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9217618/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40497203","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":"Heme Oxygenase 1/Peroxisome Proliferator-Activated Receptor Gamma Pathway Protects Intimal Hyperplasia and Mitigates Arteriovenous Fistula Dysfunction by Regulating Oxidative Stress and Inflammatory Response.","authors":"Tingfei Xie,&nbsp;Yunpeng Xu,&nbsp;Lecai Ji,&nbsp;Xiaolu Sui,&nbsp;Aisha Zhang,&nbsp;Yanzi Zhang,&nbsp;Jihong Chen","doi":"10.1155/2022/7576388","DOIUrl":"https://doi.org/10.1155/2022/7576388","url":null,"abstract":"<p><strong>Purpose: </strong>An arteriovenous fistula (AVF) is the preferred vascular access mode for maintenance hemodialysis, and access stenosis and thrombosis are the primary causes of AVF dysfunction. This study is aimed at exploring the molecular mechanisms underlying AVF development and the roles of the heme oxygenase 1/peroxisome proliferator-activated receptor gamma (HO-1/PPAR-<i>γ</i>) pathway in AVF.</p><p><strong>Method: </strong>AVF model mice were established, and the vascular tissues from the arteriovenous anastomosis site were sent for mRNA sequencing. Differentially expressed mRNAs (DEmRNAs) were screened and subjected to functional analysis. Thereafter, the mice with HO-1 knockdown and coprotoporphyrin IX chloride (COPP) pretreatment were used to investigate the roles of the HO-1/PPAR-<i>γ</i> pathway in AVF.</p><p><strong>Results: </strong>By sequencing, 2514 DEmRNAs, including 1323 upregulated and 1191 downregulated genes, were identified. These DEmRNAs were significantly enriched in the PPAR signaling pathway, AMPK signaling pathway, glucagon signaling pathway, IL-17 signaling pathway, and Toll-like receptor signaling pathway. High expression of HO-1 and PPAR-<i>γ</i> reduced endothelial damage and intimal hyperplasia during AVF maturation. After AVF was established, the levels of transforming growth factor-<i>β</i> (TGF-<i>β</i>), interleukin-1<i>β</i> (IL-1<i>β</i>), interleukin-18 (IL-18), and reactive oxygen species (ROS) were significantly increased (<i>P</i> < 0.05), and <i>HO-1</i> normal expression and COPP pretreatment evidently decreased their levels in AVF (<i>P</i> < 0.05). Additionally, AVF significantly upregulated HO-1 and PPAR-<i>γ</i> and downregulated MMP9, and COPP pretreatment and HO-1 normal expression further upregulated and downregulated their expression.</p><p><strong>Conclusion: </strong>The HO-1/PPAR-<i>γ</i> pathway may suppress intimal hyperplasia induced by AVF and protect the intima of blood vessels by regulating MMP9 and ROS, thus mitigating AVF dysfunction.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2022-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9207017/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40580732","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 Effects of High-Intensity Interval Training on Exercise Capacity and Prognosis in Heart Failure and Coronary Artery Disease: A Systematic Review and Meta-Analysis.","authors":"Cuihua Wang,&nbsp;Jun Xing,&nbsp;Baoli Zhao,&nbsp;Yahui Wang,&nbsp;Lizhuang Zhang,&nbsp;Yebo Wang,&nbsp;Mingqi Zheng,&nbsp;Gang Liu","doi":"10.1155/2022/4273809","DOIUrl":"https://doi.org/10.1155/2022/4273809","url":null,"abstract":"<p><strong>Objective: </strong>The purpose of this study is to compare the effects of high-intensity interval training (HIIT) versus moderate-intensity continuous training (MICT) on exercise capacity and several prognostic markers in patients with coronary artery disease (CAD) and heart failure (HF).</p><p><strong>Methods: </strong>This systematic review is registered on the INPLASY website (number: INPLASY202080112). We conducted a comprehensive search in eight databases of literature before September 13, 2019. Trials comparing HIIT and MICT in participants with CAD or HF aged 52-78 years were included. Exercise capacity (peak oxygen consumption (peak VO₂)) and prognostic markers, such as the anaerobic threshold (AT), minute ventilation/carbon dioxide production (VE/VCO₂) slope, left ventricular ejection fraction (LVEF), and prognostic value of the predicted VO₂ max per cent (the predicted VO₂ peak (%)) were examined.</p><p><strong>Results: </strong>A total of 15 studies were included comprising 664 patients, 50% of which were male, with an average age of 60.3 ± 13.2 years. For patients with CAD, HIIT significantly improved peak VO₂ values (95% CI 0.7 to 2.11) compared with MICT, but peak VO₂ values in patients with HF did not seem to change. For training lasting less than eight weeks, HIIT significantly improved peak VO₂ values (95% CI 0.70 to 2.10), while HIIT lasting 12 weeks or longer resulted in a modestly increased peak VO₂ value (95% CI 0.31 to 5.31). High-intensity interval training significantly increased the AT when compared with MICT (95% CI 0.50 to 1.48). High-intensity interval training also caused a moderate increase in LVEF (95% CI 0.55 to 5.71) but did not have a significant effect on the VE/VCO₂ slope (95% CI -2.32 to 0.98) or the predicted VO₂ peak (95% CI -2.54 to 9.59) compared with MICT.</p><p><strong>Conclusions: </strong>High-intensity interval training is an effective therapy for improving peak VO₂ values in patients with CAD. High-intensity interval training in the early stage (eight weeks or fewer) is superior to MICT. Finally, HIIT significantly improved prognostic markers, including the AT and LVEF in patients with CAD and HF.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2022-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9203221/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40481092","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":"Effectiveness and Safety of Nonvitamin K Oral Anticoagulants Rivaroxaban and Apixaban in Patients with Venous Thromboembolism: A Meta-Analysis of Real-World Studies.","authors":"Olivia Wu, Stephen Morris, Torben Bjerregaard Larsen, Flemming Skjøth, Alex Evans, Kevin Bowrin, Piotr Wojciechowski, Wojciech Margas, Maria Huelsebeck","doi":"10.1155/2022/2756682","DOIUrl":"10.1155/2022/2756682","url":null,"abstract":"<p><strong>Background: </strong>Rivaroxaban and apixaban are the most widely used nonvitamin K oral anticoagulants (NOACs) in patients with venous thromboembolism (VTE). This meta-analysis evaluates the effectiveness and safety of both NOACs versus standard of care (SoC) in real-world practice.</p><p><strong>Methods: </strong>Real-world evidence (RWE) studies were identified through a systematic literature review conducted between January 2012 and July 2020, using Embase, MEDLINE, and the websites of cardiological, hematological, and oncological associations. Eligible RWE studies recruited adult patients with deep vein thrombosis and/or pulmonary embolism and presented a comparison between rivaroxaban and apixaban versus SoC, consisting either of vitamin K antagonists, heparins, or combinations thereof. Hazard ratios (HRs) for the comparison between NOACs and SoC were extracted from the relevant studies or estimated based on the reported binary data. The between-treatment contrasts were reported as HRs with associated 95% confidence intervals.</p><p><strong>Results: </strong>A total of 65 RWE studies were identified and considered relevant for the meta-analysis. Compared with SoC, both rivaroxaban and apixaban were associated with reduced risks of recurrent VTE and a lower rate of major bleeding events. Patients treated with rivaroxaban were at a lower risk of all-cause death compared with those receiving SoC (HR = 0.56 [0.39-0.80]), while evidence for apixaban from the identified studies was insufficient to demonstrate a statistically significant change in mortality (HR = 0.66 [0.30-1.47]).</p><p><strong>Conclusion: </strong>This analysis indicates that in real-world practice, rivaroxaban and apixaban are associated with a lower risk of recurrent VTE and major bleeding events compared with SoC. Survival benefit in patients treated with rivaroxaban was also observed.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2022-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9203223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40481093","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":"Thymosin β4 Protects against Cardiac Damage and Subsequent Cardiac Fibrosis in Mice with Myocardial Infarction","authors":"Fei Wang, Yajuan He, N. Yao, L. Ruan, Z. Tian","doi":"10.1155/2022/1308651","DOIUrl":"https://doi.org/10.1155/2022/1308651","url":null,"abstract":"Background Inflammation is a critical factor in the development and progression of myocardial infarction and cardiac fibrosis. Thymosin β4 (Tβ4) alleviates the disease process via protective antioxidant and anti-inflammatory mechanisms. Although Tβ4 has been shown to have a protective effect in myocardial infarction, its impact on cardiac fibrosis has not been well reported. In this study, we evaluated the influence of exogenous Tβ4 on myocardial infarction and cardiac fibrosis and explored the possible underlying mechanism. Methods Real-time quantitative reverse-transcription PCR (qRT-PCR), immunohistochemistry (IHC), and Western blot were used to analyze Tβ4 expression in acute myocardial infarction (AMI) cardiac tissues. The effects of intraperitoneal adeno-associated virus-Tβ4 (AAV-Tβ4) on ligation-induced AMI in mice were studied using cardiac function parameters, and RT-PCR, Western blot, HE staining, Masson staining, and IHC were used to assess the degree of myocardial fibrosis. The effects of Tβ4 were confirmed in vitro using mouse cardiac myocytes and myofibroblasts. Results Tβ4 was shown to be significantly elevated in mice AMI cardiac tissues. In mice, AAV-Tβ4 induced exogenous expression of Tβ4 significantly reduced oxidative damage, inflammation, cardiac dysfunction, and fibrosis. H2O2 inhibited mitophagy and increased inflammation in mouse cardiac myocytes via oxidative stress, and Tβ4 substantially reduced mitophagy inhibition and inflammasome activation in myocytes caused by H2O2. Furthermore, Tβ4 decreased cardiac myofibroblast growth and reduced TGF-β1-induced activation. Conclusions AAV-Tβ4 induced expression of Tβ4 reduced inflammation, heart damage, and eventual fibrosis in vivo. Tβ4 helped to reduce oxidative stress, promote mitophagy, and alleviate inflammation and fibrosis. Exogenous supplementation of Tβ4 might be a promising therapeutic agent for treating myocardial infarction as well as cardiac fibrosis.","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2022-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48808052","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":"MIR22HG Aggravates Oxygen-Glucose Deprivation and Reoxygenation-Induced Cardiomyocyte Injury through the miR-9-3p/SH2B3 Axis","authors":"Yi Ge, Lishi Liu, L. Luo, Yu Fang, Tong Ni","doi":"10.1155/2022/7332298","DOIUrl":"https://doi.org/10.1155/2022/7332298","url":null,"abstract":"Reperfusion therapy, the standard treatment for acute myocardial infarction (MI), can trigger necrotic death of cardiomyocytes and provoke ischemia/reperfusion (I/R) injury. However, molecular mechanisms that regulate cardiomyocyte death remain largely unknown. The abnormal expression of lncRNA MIR22HG has been found in types of diseases. The current study was aimed at exploring the function and mechanism of MIR22HG in I/R injury. In this study, mouse myocardial cells (HL-1) treated with oxygen-glucose deprivation and reoxygenation (OGD/R) were used as the in vitro models, and myocardial ischemia reperfusion injury (MIRI) animal models in vivo were established in male C57BL/6 mice. Experiments including CCK-8, flow cytometry, TUNEL, HE staining, RT-qPCR, western blotting, and luciferase reporter assays were performed to explore the function and potential mechanism of MIR22HG in MIRI in vitro and in vivo. Bioinformatics analysis was performed to predict the binding site between miR-9-3p and MIR22HG (or SH2B3). Our results indicated that the MIR22HG level was upregulated in cardiomyocytes after OGD/R treatment. The knockdown of MIR22HG promoted cell viability and inhibited apoptosis and extracellular matrix (ECM) production in OGD/R-treated HL-1 cells. In mechanism, MIR22HG binds to miR-9-3p, and miR-9-3p targets the SH2B3 3′ untranslated region (UTR). Moreover, SH2B3 expression was positively regulated by MIR22HG but negatively modulated by miR-9-3p. Rescue assays suggested that the suppressive effect of MIR22HG knockdown on cell viability, apoptosis, and ECM accumulation was reversed by the overexpression of SH2B3. The in vivo experiments demonstrated that MIR22HG knockdown alleviated cardiomyocyte apoptosis and reduced myocardial infarct size in MIRI mice. In summary, MIR22HG knockdown alleviates myocardial injury through the miR-9-3p/SH2B3 axis.","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2022-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46511192","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}