Cardiovascular Therapeutics最新文献

{"title":"Heparin and Bivalirudin in Percutaneous Coronary Intervention for Acute Coronary Syndromes: A Review Article","authors":"Guiping Wang,&nbsp;Kaijie Qi,&nbsp;Xuyang Li,&nbsp;Shuping Zuo,&nbsp;Ruolin Zhang,&nbsp;Yanan Zhao,&nbsp;Suya Sun,&nbsp;Juanjuan Zhang,&nbsp;Xiaokun Liu","doi":"10.1155/cdr/5549914","DOIUrl":"10.1155/cdr/5549914","url":null,"abstract":"<p>Acute coronary syndrome (ACS) is one of the most common leading global causes of mortality, encompassing ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina (UA). Percutaneous coronary intervention (PCI) has become a pivotal therapeutic approach for ACS, underscoring the importance of anticoagulation strategies. Among the commonly employed anticoagulants in PCI, heparin and bivalirudin take precedence, with heparin serving as the archetypal choice. Nevertheless, the determination of an optimal anticoagulation regimen remains a point of contention in contemporary clinical practice. To address the differences in anticoagulants during PCI, we meticulously conducted a literature review through PubMed and Web of Science, employing search terms such as “heparin,” “bivalirudin,” “percutaneous coronary intervention,” and “acute coronary syndrome.” For patients with PIC brought on by STEMI, NSTEMI, and stable or UA pectoris, the review focused on randomized controlled trials to assess and compare the efficacy and safety of heparin and bivalirudin as anticoagulant options. This systematic review is aimed at furnishing valuable insights into the ongoing debate surrounding the choice of anticoagulation regimens in PCI. By scrutinizing clinical evidence derived from relevant trials, we seek to inform and guide healthcare practitioners in making informed decisions based on the unique requirements of patients with various ACS presentations.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2024 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11695083/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920889","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":"Thymidine Phosphorylase Promotes Abdominal Aortic Aneurysm via VSMC Modulation and Matrix Remodeling in Mice and Humans","authors":"Liang Hong,&nbsp;Hong Yue,&nbsp;Dunpeng Cai,&nbsp;Autumn DeHart,&nbsp;Gretel Toloza-Alvarez,&nbsp;Lili Du,&nbsp;Xianwu Zhou,&nbsp;Xiaoping Fan,&nbsp;Huanlei Huang,&nbsp;Shiyou Chen,&nbsp;Shaik O. Rahaman,&nbsp;Jian Zhuang,&nbsp;Wei Li","doi":"10.1155/cdr/1129181","DOIUrl":"https://doi.org/10.1155/cdr/1129181","url":null,"abstract":"<p><b>Background:</b> Thymidine phosphorylase (TYMP) promotes platelet activation and thrombosis while suppressing vascular smooth muscle cell (VSMC) proliferation. Both processes are central to the development and progression of abdominal aortic aneurysms (AAAs). We hypothesize that TYMP plays a role in AAA development.</p><p><b>Methods:</b> Male wild-type (WT) C57BL/6J and <i>Tymp^−/−</i> mice, fed a Western diet (WD) (TD.88137), were subjected to the 4-week Ang II infusion–induced AAA model. AAA progression was monitored by echography and confirmed through necropsy. Whole-body inflammation was assessed using a plasma cytokine array. Mechanistic studies were conducted using TYMP-overexpressing rat VSMC cell lines and primary VSMCs cultured from WT and <i>Tymp^−/−</i> mouse thoracic aortas. Histological studies were performed on human AAA and normal aorta samples.</p><p><b>Results:</b> Elevated TYMP levels were observed in human AAA vessel walls. While WT mice exhibited a 28.6% prevalence of Ang II infusion–induced AAA formation, <i>Tymp^−/−</i> mice were protected. TYMP enhanced MMP2 expression, secretion, and activation in VSMCs, which was inhibited by tipiracil, a selective TYMP inhibitor. Systemically, TYMP promoted proinflammatory cytokine expression, and its absence attenuated TNF-<i>α</i>-induced MMP2 and AKT activation. WT VSMCs treated with platelets lacking TYMP showed a higher proliferation rate than cells treated with WT platelets. Additionally, TYMP increased activated TGF<i>β</i>1 expression in cultured VSMCs and human AAA vessel walls. In WT VSMCs, TYMP augmented thrombospondin-1 type 1 repeat domain (TSR)–stimulated TGF<i>β</i>1 signaling, increasing connective tissue growth factor and MMP2 production. TSR also enhanced AKT activation in WT VSMCs but had the opposite effect in <i>Tymp^−/−</i> cells. TSR-enhanced MMP2 activation in WT VSMCs was attenuated by LY294002 (a PI3K inhibitor) but not by SB431542 (a TGF<i>β</i>1 inhibitor); both inhibitors had indiscernible effects on <i>Tymp^−/−</i> VSMC.</p><p><b>Conclusion:</b> TYMP emerges as a novel regulatory force in vascular biology, influencing VSMC function and inflammatory responses to promote AAA development.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2024 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/1129181","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142861864","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":"Application of the Left Ventricular Pressure–Strain Loop Technique in Monitoring Improvement Factors of Patients With Heart Failure Reduced Ejection Fraction","authors":"Qing Li,&nbsp;Yaolei Guo,&nbsp;Xiaomin Tang,&nbsp;Chang Liu,&nbsp;Zhidong Wang,&nbsp;Qianping Gao,&nbsp;Yuanshi Li,&nbsp;Junxian Cao","doi":"10.1155/cdr/5562513","DOIUrl":"https://doi.org/10.1155/cdr/5562513","url":null,"abstract":"<p>The left ventricular pressure–strain loop (PSL) is a new technique based on ultrasound for noninvasive quantitative evaluation of global and local myocardial work (MW). This study is aimed at evaluating improvement factors of patients with heart failure (HF) reduced ejection fraction (HFrEF) using the PSL technique. A total of 88 patients with HF were enrolled in this study, which had ≤ 40% left ventricular ejection fraction (LVEF). The EchoPAC workstation was used to obtain the global longitudinal strain (GLS) and MW parameters of the left ventricle. All patients have taken medicines for HF treatments for 6–12 months. The improvements of HF after therapies were evaluated according to the following recommended criteria. The clinical characteristics of patients with improved and nonimproved groups were stratified via univariate or multivariate logistic regression analysis, receiver operating characteristic (ROC), and the area under ROC (area under the curve (AUC)). There were no significant differences in general medical information, the underlying diseases, laboratory findings, myocardial enzyme activities, and taking medicines between the improved and nonimproved LVEF patients (<i>p</i> &gt; 0.05). There were significant differences in LVEF of patients at admission, left ventricular end-diastolic diameter (LVEDD), interventricular septum thickness (IVST), early diastolic mitral flow peak velocity E (E peak), GLS, global myocardial work index (GWI), global myocardial constructive work (GCW), and global myocardial work efficiency (GWE) between the two groups (<i>p</i> &lt; 0.05). Univariate and multivariate logistic regression analyses confirmed that GWI and GCW were critical predictive factors for LVEF improvement in patients with HF. ROC curve showed that the AUC of GWI and GCW were 0.796 and 0.779 at the cut-off of 741 mmHg% for GWI and 973.5 mmHg% for GCW, respectively. The sensitivities of GWI and GCW were 65% and 75%, and the specificities of GWI and GCW were 83.3% and 79.2% at given cut-off values. These results revealed that GWI and GCW were independent predictors of improvement of LVEF in patients with HFrEF.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2024 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/5562513","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142861847","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":"DJ-1 as a Novel Therapeutic Target for Mitigating Myocardial Ischemia–Reperfusion Injury","authors":"Jia-Bin Zhou,&nbsp;Tian-Peng Wei,&nbsp;Dan Wu,&nbsp;Feng Zhou,&nbsp;Ru-Xing Wang","doi":"10.1155/cdr/6615720","DOIUrl":"https://doi.org/10.1155/cdr/6615720","url":null,"abstract":"<p>Ischemic heart disease (IHD) remains one of the most prominent causes of mortality and morbidity globally, and the risk of ischemia–reperfusion injury is becoming more severe and constant. This underscores the need to develop new methods to protect the heart from damage. DJ-1 is a multifunctional intracellular protein encoded by the <i>PARK7</i> gene that plays roles in processes including the control of autophagy, the preservation of mitochondrial integrity, the prevention of apoptosis, and the elimination of oxidative stress. DJ-1 has recently been the focus of growing interest as a target molecule relevant to treating myocardial ischemia–reperfusion injury due to its protective properties and its role in cellular response mechanisms. Consistently, DJ-1-related interventions, such as its exogenous administration or the use of pharmacological agents, have been demonstrated to help protect the myocardium from ischemia–reperfusion injury and associated adverse outcomes. This review provides an overview of DJ-1 and its therapeutic relevance in the myocardium in the setting of ischemia and reperfusion.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2024 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/6615720","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142861294","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":"Dehydroevodiamine Alleviates Doxorubicin-Induced Cardiomyocyte Injury by Regulating Neuregulin-1/ErbB Signaling","authors":"Song Jie,&nbsp;Guo Wenying,&nbsp;Sun Lebo","doi":"10.1155/cdr/5538740","DOIUrl":"https://doi.org/10.1155/cdr/5538740","url":null,"abstract":"<p><b>Background:</b> Doxorubicin (DOX) is a widely used antitumor drug; however, its use is limited by the risk of serious cardiotoxicity. Dehydroevodiamine (DHE) is a quinazoline alkaloid which has antiarrhythmic effects. The aim of this study was to investigate the protective effect of DHE on doxorubicin-induced cardiotoxicity (DIC) and its potential mechanism.</p><p><b>Materials and Methods:</b> Rat H9c2 cardiomyocytes were exposed to DOX for 24 h to establish a DOX-induced cardiomyocyte injury model. DHE and ErbB inhibitor AG1478 were used to treat H9c2 cells to investigate their effects. Cell counting kit-8 (CCK-8) and lactate dehydrogenase (LDH) release assays were used to evaluate cell viability. Flow cytometry and caspase-3 activity assay were used to detect apoptosis. Western blot was used to detect the expression levels of apoptosis-related proteins and neuregulin-1 (NRG1)/ErbB pathway–related proteins. The levels of proinflammatory cytokines and markers of oxidative stress were also detected, respectively. Quantitative polymerase chain reaction (qPCR) was used to detect mRNA expression levels of hub genes.</p><p><b>Results:</b> DHE enhanced cardiomyocyte viability and decreased LDH release in a concentration- and time-dependent manner. DHE also significantly inhibited DOX-induced cardiomyocyte apoptosis, inflammation, and oxidative stress. Bioinformatics analysis showed that the protective mechanism of DHE against DIC was related to ErbB signaling pathway. DOX treatment significantly reduced NRG1, p-ErbB2, and p-ErbB4 protein expression levels in cardiomyocytes, while DHE pretreatment reversed this effect. ErbB inhibitor AG1478 reversed the protective effect of DHE on cardiomyocytes.</p><p><b>Conclusion:</b> DHE protects cardiomyocytes against DOX by regulating NRG1/ErbB pathway. DHE may be a potential agent for the prevention and treatment of DIC.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2024 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/5538740","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142860350","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":"Cysteine Leukotriene Receptor Antagonist—Montelukast—Treatment Improves Experimental Abdominal Aortic Aneurysms in Mice","authors":"Kexin Li,&nbsp;Meng Li,&nbsp;Panpan Wei,&nbsp;Kangli Tian,&nbsp;Haole Liu,&nbsp;Weilai Fu,&nbsp;Haiwen Hou,&nbsp;Yajie Chen,&nbsp;Baohui Xu,&nbsp;Yankui Li,&nbsp;Sihai Zhao","doi":"10.1155/2024/8826287","DOIUrl":"https://doi.org/10.1155/2024/8826287","url":null,"abstract":"<p><b>Background:</b> Cysteinyl leukotrienes (LTs) and their receptors are involved in the pathogenesis of abdominal aortic aneurysms (AAAs). However, whether CysLT1 receptor antagonists such as montelukast can influence experimental nondissecting AAA remains unclear.</p><p><b>Methods:</b> Nondissecting AAAs were induced in C57BL/6J mice by transient aortic luminal infusion of porcine pancreatic elastase (PPE). All animals were administrated montelukast (1 or 10 mg/kg, daily) or vehicle by gavage beginning 1 day before PPE infusion for 14 days. On day 0 (baseline) and day 14 after PPE infusion, abdominal aortic diameters were directly measured. Aortic aneurysmal segment samples were collected, and histopathological analysis was performed.</p><p><b>Results:</b> Compared to vehicle treatment, montelukast significantly decreased PPE infusion–induced aortic expansion in a dose-dependent manner (0.09-mm reduction at a low dose and 0.19-mm reduction at a high dose). Histopathological analysis also revealed that compared with vehicle treatment, montelukast treatment, especially in the high-dose group, significantly improved PPE-induced aortic elastin degradation and medial smooth muscle cell depletion. Both doses of montelukast also markedly decreased the number of local leucocytes, including macrophages, CD4⁺ T cells, CD8⁺ T cells, and B cells, infiltration and accumulation in aortic aneurysmal lesions. Montelukast treatment also downregulated matrix metalloproteinase 2 (MMP2) and MMP9 expression and inhibited mural angiogenesis in aneurysmal aortas.</p><p><b>Conclusion:</b> Montelukast treatment improves experimental nondissected AAAs in mice partly by improving aortic inflammation.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2024 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2024/8826287","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142724218","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":"Angiotensin Receptor–Neprilysin Inhibitor in Heart Failure Patients With Renal Dysfunction","authors":"Xiaogang Zhu,&nbsp;Xialing Li,&nbsp;Lingxuan Zhu,&nbsp;Zichuan Tong,&nbsp;Xiuying Xu","doi":"10.1155/2024/6231184","DOIUrl":"https://doi.org/10.1155/2024/6231184","url":null,"abstract":"<p>Heart failure (HF) and renal dysfunction often coexist and interact in many complex and bidirectional pathways, leading to detrimental effects on patient outcomes. The treatment of HF patients with renal dysfunction presents a significant clinical challenge. Interestingly, sacubitril/valsartan, an angiotensin receptor–neprilysin inhibitor (ARNI), may have beneficial effects on cardiac and renal outcomes in patients with HF with reduced ejection fraction, particularly by slowing the rate of decrease in the estimated glomerular filtration rate compared to a single angiotensin–converting enzyme inhibitor. Recently, more reports have emphasized the renal protection of sacubitril/valsartan in patients with HF. In HF patients with renal dysfunction, however, there is no strong evidence supporting the use of sacubitril/valsartan to reduce the absolute risk of hyperkalemia and worsening renal function; therefore, the administration of ARNI requires a careful balance between the benefits and risks. Furthermore, the lack of evidence-based management highlights the importance of an individualized approach based on published experience and multidisciplinary collaborations, as well as underlines the need for in-depth studies investigating the underlying mechanisms in cardiorenal interactions with a focus on treatments.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2024 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2024/6231184","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142573915","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":"Overexpression of TRPV6 Inhibits Coronary Atherosclerosis–Related Inflammatory Response and Cell Apoptosis via the PKA/UCP2 Pathway","authors":"Lei Zheng,&nbsp;Huiying Zhang,&nbsp;Xuewen Li","doi":"10.1155/2024/7053116","DOIUrl":"https://doi.org/10.1155/2024/7053116","url":null,"abstract":"<p><b>Objective:</b> This research is aimed at unravelling the intricate relationship between transient receptor potential vanilloid 6 (TRPV6), protein kinase A (PKA), uncoupling protein 2 (UCP2), and atherosclerosis. By shedding light on the role of the TRPV6/PKA/UCP2 pathway in inhibiting inflammatory response and cell apoptosis in coronary atherosclerotic plaques, this study provides valuable insights into potential therapeutic targets for treating coronary artery disease (CAD).</p><p><b>Methods:</b> We established animal and cell models of atherosclerosis. The expression of TRPV6 was measured using immunohistochemistry and immunofluorescence. Cytokine levels were detected by enzyme-linked immunosorbent assay (ELISA). Cell viability and apoptosis ratio were measured using cell counting kit-8 (CCK-8) and flow cytometry. The binding relationship between TRPV6 and PKA was validated using chromatin immunoprecipitation (CHIP) and coimmunoprecipitation (CoIP). Finally, the expression of the TRPV6/PKA/UCP2 signaling pathway and apoptosis-related factors was detected using western blot (WB) and quantitative real-time polymerase chain reaction (qRT-PCR).</p><p><b>Results:</b> TRPV6 was significantly decreased in atherosclerosis mouse and cell model. CHIP and CoIP assays indicated that TRPV6 binds to PKA and positively regulated its expression in oxidized low-density lipoprotein (ox-LDL)–treated human umbilical vein endothelial cells (HUVECs). Overexpression of TRPV6 significantly increased cell viability and inhibited apoptosis, whereas silencing TRPV6 had the opposite effect. Additionally, the overexpression of TRPV6 remarkably declined the expression of tumor necrosis factor-alpha (TNF-<i>α</i>), interleukin-6 (IL-6), and interleukin-1 beta (IL-1<i>β</i>). However, after silencing PKA, this effect was partially reversed, the cell viability and inflammatory response remarkably enhanced, and apoptosis significantly declined in oe-TRPV6 + si-PKA group.</p><p><b>Conclusions:</b> In summary, our study demonstrated that TRPV6 inhibited apoptosis and inflammatory response in the atherosclerosis cell model through the regulation of the PKA/UCP2 pathway.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2024 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2024/7053116","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142525216","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 Bioprotective Effects of Marigold Tea Polyphenols on Obesity and Oxidative Stress Biomarkers in High-Fat-Sugar Diet-Fed Rats","authors":"Bader Alsuwayt,&nbsp;Neelam Iftikhar,&nbsp;Abdullah Ijaz Hussain,&nbsp;Ashfaq Ahmad,&nbsp;Irsa Zafar,&nbsp;Arifa Khanam,&nbsp;Wen-Nee Tan,&nbsp;Lutfun Nahar,&nbsp;Afaf F. Almuqati,&nbsp;Esraa Mohammad Haji,&nbsp;Ali F. Almutairy,&nbsp;Satyajit D. Sarker","doi":"10.1155/2024/3833521","DOIUrl":"https://doi.org/10.1155/2024/3833521","url":null,"abstract":"<p><b>Background:</b> The research is aimed at exploring the potential of marigold petal tea (MPT), rich in polyphenol contents, against oxidative stress and obesity in a rat model following a high-fat-sugar diet (HFSD).</p><p><b>Methods:</b> The MPT was prepared through the customary method of decoction and was subjected to analysis for its polyphenol composition using reversed-phase high-performance liquid chromatography (RP-HPLC). Two specific doses of MPT, namely, 250 and 500 mg/kg body weight (BW), were chosen for the study—referred to as MPT-250 and MPT-500, respectively.</p><p><b>Result:</b> The main phenolic acids and flavonoids identified in MPT, with concentrations exceeding 10 mg/100 mL of tea, included catechin, rutin, salicylic acid, gallic acid, sinapic acid, chlorogenic acid, cinnamic acid, and ellagic acid. The total phenolic (TP) and total flavonoid (TF) contents in MPT were measured to be 5.53 and 7.73 mg/g, respectively. Additionally, MPT demonstrated a 57.2% scavenging capacity with 2,2-diphenyl-1-picrylhydrazyl radical. Notably, the administration of a higher dose (MPT-500) showed a significant reduction in body mass index (BMI) and a 51.24% reduction in the rate of increase in BW compared to the HFSD group. The findings indicated that all the treatment groups, that is, orlistat treatment (OT), MPT-250, and MPT-500 groups, experienced reduced levels of serum total cholesterol (TC), triglyceride (TG), and markers of lipoproteins in contrast to the HFSD group. Moreover, MPT helped restore the levels of malondialdehyde (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH), thereby demonstrating its potential in combating oxidative stress. The MPT-500 group also displayed decreased liver and kidney weights and an improved atherogenic index when compared to the HFSD group.</p><p><b>Conclusion:</b> The results clearly indicate that a high dosage of MPT showed antiobesity activity which was comparable to the same effects produced by the conventional drug orlistat.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2024 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2024/3833521","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142404138","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 Network and Pathway Analysis of Genes Associated With Atrial Fibrillation","authors":"Mengying Zeng,&nbsp;Xian Yang,&nbsp;Yunhao Chen,&nbsp;Jinqi Fan,&nbsp;Li Cao,&nbsp;Menghao Wang,&nbsp;Peilin Xiao,&nbsp;Zhiyu Ling,&nbsp;Yuehui Yin,&nbsp;Yunlin Chen","doi":"10.1155/2024/7054039","DOIUrl":"https://doi.org/10.1155/2024/7054039","url":null,"abstract":"<p><b>Background:</b> Atrial fibrillation (AF) is affected by both environmental and genetic factors. Previous genetic association studies, especially genome-wide association studies, revealed a large group of AF-associated genes. However, little is known about the functions and interactions of these genes. Moreover, established genetic variants of AF contribute modestly to AF variance, implying that numerous additional AF-associated genetic variations need to be identified. Hence, a systematic network and pathway analysis is needed.</p><p><b>Methods:</b> We retrieved all AF-associated genes from genetic association studies in various databases and performed integrative analyses including pathway enrichment analysis, pathway crosstalk analysis, network analysis, and microarray meta-analysis.</p><p><b>Results:</b> We collected 254 AF-associated genes from genetic association studies in various databases. Pathway enrichment analysis revealed the top biological pathways that were enriched in the AF-associated genes related to cardiac electromechanical activity. Pathway crosstalk analysis showed that numerous neuro-endocrine-immune pathways connected AF with various diseases including cancers, inflammatory diseases, and cardiovascular diseases. Furthermore, an AF-specific subnetwork was constructed with the prize-collecting Steiner forest algorithm based on the AF-associated genes, and 24 novel genes that were potentially associated with AF were inferred by the subnetwork. In the microarray meta-analysis, six of the 24 novel genes (<i>APLP1</i>, <i>CREB1</i>, <i>CREBBP</i>, <i>PRMT1</i>, <i>IRAK1</i>, and <i>PLXND1</i>) were expressed differentially in patients with AF and sinus rhythm.</p><p><b>Conclusions:</b> AF is not only an isolated disease with abnormal electrophysiological activity but might also share a common genetic basis and biological process with tumors and inflammatory diseases as well as cardiovascular diseases. Moreover, the six novel genes inferred from network analysis might help detect the missing AF risk loci.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2024 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2024/7054039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142404286","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}