Cardiovascular Therapeutics最新文献

{"title":"Outcomes of 10 mg Rivaroxaban in Nonvalvular Atrial Fibrillation Patients With CrCl ≥ 50 mL/min: A Retrospective Cohort Study","authors":"Qing Yan,&nbsp;Yide Yuan,&nbsp;Jiaqi Liang,&nbsp;Yuyang Zhao,&nbsp;Yuan Li,&nbsp;Jiali Fan,&nbsp;Jiahong Xue,&nbsp;Qiangsun Zheng","doi":"10.1155/cdr/7021330","DOIUrl":"https://doi.org/10.1155/cdr/7021330","url":null,"abstract":"<p><b>Background:</b> The standard oral dose of rivaroxaban for nonvalvular atrial fibrillation (NVAF) patients with a creatinine clearance rate (CrCl) ≥ 50 m<i>L</i>/min is 20 mg/day in Europe and 15 mg/day in Japan. In the real world, low-dosing (10 mg/day) rivaroxaban has been widely used in clinical practice in China due to bleeding concerns. However, the impact of low-dose rivaroxaban on clinical outcomes remains uncertain.</p><p><b>Methods:</b> This retrospective study included NVAF patients with CrCl ≥ 50 mL/min treated at the Second Affiliated Hospital of Xi’an Jiaotong University from January 2017 to June 2022. Patients were divided into two groups: standard-dose (15 or 20 mg/day) and low-dose (10 mg/day). Inverse probability of treatment weighting (IPTW) was used to balance baseline characteristics. The risk of ischemic stroke (IS)+systemic embolism (SE) and bleeding was compared between the two groups by survival analysis.</p><p><b>Results:</b> A total of 1455 patients (mean age: 66.98 ± 11.16 years; 55.95% female) were included. In the low-dose group (<i>n</i> = 1176), 78 (6.63%) experienced IS/SE and 68 (5.78%) had bleeding. In the standard-dose group (<i>n</i> = 279), 13 (4.66%) experienced IS/SE and 18 (6.45%) had bleeding. Cox regression suggested that compared to the standard-dose group, patients in the low-dose group did not show a significantly different risk of IS+SE (HR = 1.01, 95% CI: 0.51–1.96, <i>p</i> = 0.999) or bleeding (HR = 0.90, 95% CI: 0.49–1.67, <i>p</i> = 0.749). Subgroup analysis revealed that for patients with BMI &lt; 24 kg/m², low-dose rivaroxaban reduced bleeding risk (HR = 0.53, 95% CI: 0.29–0.99, <i>p</i> = 0.049).</p><p><b>Conclusion:</b> For NVAF patients with CrCl ≥ 50 mL/min in China, low-dose rivaroxaban (10 mg/day) is a viable alternative to standard doses in preventing IS/SE. In nonoverweight patients (BMI &lt; 24 kg/m²), it offers comparable efficacy with enhanced safety.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/7021330","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493030","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":"Antagonizing CCR2 With Propagermanium Leads to Altered Distribution of Macrophage Subsets and Favorable Tissue Remodeling After Myocardial Infarction in Mice","authors":"Kay Weipert,&nbsp;Holger Nef,&nbsp;Sandra Voss,&nbsp;Jedrzej Hoffmann,&nbsp;Sven Reischauer,&nbsp;Andreas Rolf,&nbsp;Kerstin Troidl,&nbsp;Astrid Wietelmann,&nbsp;Christian W. Hamm,&nbsp;Samuel T. Sossalla,&nbsp;Christian Troidl","doi":"10.1155/cdr/8856808","DOIUrl":"https://doi.org/10.1155/cdr/8856808","url":null,"abstract":"<p><b>Aims:</b> The aim of the present study was to investigate the inhibition of classically activated macrophages in myocardial infarction (MI) under the influence of the chemokine (C-C motif) receptor 2 (CCR2) antagonist propagermanium (PPG).</p><p><b>Methods and Results:</b> Mice (C57BL/6; <i>n</i> = 121) were subjected to occlusion of the left anterior descending artery and were randomized to the following groups: (a) MI with daily oral administration of 0.9% sodium chloride (“MI”), (b) MI with oral administration of 8 mg/kg PPG (“MI + PPG”), and (c) sham-operated mice served as control. Mice were euthanized 2, 5, 10, or 21 days after MI for isolation of total RNA, protein, and immunofluorescence measurements. Flow cytometry was performed to investigate peripheral blood leucocytes. Scar size and cardiac function were determined by MRI on Day 7 after surgery and by trichrome staining on Day 21. PPG administration led to a significantly improved ejection fraction (MI + PPG: 38.5<i>%</i> ± 3.4<i>%</i> vs. MI: 23.8<i>%</i> ± 3.0<i>%</i>; <i>p</i> &lt; 0.05) after MI. MRI also revealed improved wall thickness (34.7<i>%</i> ± 3.2<i>%</i> vs. 21.8<i>%</i> ± 2.9<i>%</i>; <i>p</i> &lt; 0.05) associated with a diminished akinetic area (13.8<i>%</i> ± 4.0<i>%</i> vs. 37.3<i>%</i> ± 5.6<i>%</i>; <i>p</i> &lt; 0.01). Trichrome staining confirmed less collagen scar formation in the PPG-treated group (12.7<i>%</i> ± 1.4<i>%</i> vs. 21.9<i>%</i> ± 3.9<i>%</i>; <i>p</i> &lt; 0.05). Flow cytometry showed fewer peripheral blood monocytes in MI + PPG than in MI 2 days after treatment (4.0<i>%</i> ± 0.7<i>%</i> vs. 12.7<i>%</i> ± 1.2<i>%</i> of total leucocytes; <i>p</i> &lt; 0.05). Immunostaining and western blotting using activation type-specific markers CCR2 and MRC1 demonstrated that the number of alternatively activated macrophages within the infarct zone increased, whereas the overall number was reduced after PPG treatment. PPG led to increased expression of VEGF-<i>α</i> and VEGF-<i>β</i> in THP-1 cells in vitro and increased capillary density in vivo 2 days after MI (MI-PPG: 1071 ± 81/mm² vs. MI: 648 ± 79/mm² (<i>p</i> &lt; 0.05)).</p><p><b>Conclusion:</b> Our results suggest that altering the activation type and distribution of invading macrophages in favor of alternative activation improves cardiac remodeling and function following MI.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/8856808","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144482274","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":"Trimethylamine-N-Oxide Impedes Late Endothelial Progenitor Cell–Mediated Revascularization by Triggering Mitochondrial Apoptosis via Suppression of MnSOD","authors":"Yijia Shao,&nbsp;Jiapan Sun,&nbsp;Xiang Liu,&nbsp;Xing Liu,&nbsp;Fang Wu,&nbsp;Zhichao Wang,&nbsp;Shiyue Xu,&nbsp;Long Chen","doi":"10.1155/cdr/9910333","DOIUrl":"https://doi.org/10.1155/cdr/9910333","url":null,"abstract":"<p><b>Background and Aims:</b> Trimethylamine-N-oxide (TMAO) is recognized as a novel marker and mediator of atherosclerotic cardiovascular disease (ASCVD). Endothelial progenitor cells (EPCs) are crucial for maintaining vascular homeostasis. Impaired EPC numbers and function correlate with increased adverse cardiovascular events. The aim of this study was to decipher the effect of TMAO on late EPCs (LEPCs) and its underlying molecular mechanism.</p><p><b>Methods and Results:</b> In vitro migration and tubulogenic capacities of LEPCs were attenuated by TMAO in a dose-dependent manner, accompanied by inhibition of manganese superoxide dismutase (MnSOD) and mitochondrial damage. TMAO-induced mitochondrial damage provoked proinflammatory responses (increased levels of IL-6, IL-1b, ICAM-1, E-sel, and TNF-<i>α</i>) and autophagic cell death (confirmed by western blot immunofluorescent staining and transmission electron microscopy) in LEPCs. Overexpression of MnSOD through adenovirus transfection reversed TMAO-related LEPCs dysfunction. To study the effect of TMAO on LEPC-mediated vascular repair in vivo, a hind limb ischemia model was established in nude mice, and LEPCs were injected in the ischemic hind limb. Laser Doppler imaging of mouse ischemic hindlimbs at 21 days indicated that TMAO treatment inhibited LEPCs-mediated blood flow recovery, which was restored by MnSOD overexpression. Immunohistology analyses further revealed consistent alterations in capillary density determined by CD31 staining.</p><p><b>Conclusions:</b> TMAO induces mitochondrial damage in LEPCs via MnSOD suppression, which leads to cell dysfunction, proinflammatory activation, and autophagic cell death in vitro and impaired LEPCs-mediated revascularization in vivo. Overexpression of MnSOD restores TMAO-induced LEPCs dysfunction and further enhances LEPC-mediated revascularization in the ischemic hind limbs in nude mice.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/9910333","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315076","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 Meta-Analysis of the Incidence of Adverse Reactions of Statins in Various Diseases","authors":"Wanying Li,&nbsp;Ding Wang,&nbsp;Caiyue Lin,&nbsp;Tongze Cai,&nbsp;Mei Zhao,&nbsp;Liuguan Liang,&nbsp;Xingxing Zhao,&nbsp;Xin He,&nbsp;Xiaoyue Liang,&nbsp;Jinghui Zheng","doi":"10.1155/cdr/6684099","DOIUrl":"https://doi.org/10.1155/cdr/6684099","url":null,"abstract":"<p><b>Introduction:</b> In clinical practice, patients often avoid or cease statin use due to adverse reactions or noncompliance. To elucidate statin adverse reactions, their variability across diseases, and the factors influencing them, we conducted a high-quality clinical trial–based meta-analysis.</p><p><b>Materials and Methods:</b> Clinical randomized controlled trials involving statins and detailed recording of adverse reactions in the following three databases: PubMed, Embase, and Cochrane Library were included. The retrieval was completed by January 31, 2024. All studies will use the ROB2 scale for bias risk assessment.</p><p><b>Results:</b> We had included a total of 41 studies, involving a collective sample size of 64,728 individuals. In patients with hyperlipidemia, there was no difference in the overall incidence of total adverse events among four types of statins (<i>p</i> = 0.37). Simvastatin 40 mg had fewer statin-related adverse reactions. High-dose statin users experienced no remarkable transaminase elevation 0.00201 (95% CI [0.00004, 0.00398], <i>I</i>² = 33<i>%</i>). Creatine phosphokinase (CK) elevation under three times the upper limit was rare with a rate of 0.0043 (95% CI [0.0011, 0.0075], <i>I</i>² = 27<i>%</i>). Myalgia rates were comparable between high- and moderate-dose statins (<i>p</i> = 0.23). Gastrointestinal symptoms were infrequent with a rate of about 0.02 (95% CI [0.00, 0.01], <i>I</i>² = 52<i>%</i>). For patients with coronary heart disease, pravastatin 40 mg resulted in fewer transaminase elevations (<i>p</i> &lt; 0.01). There is no difference in myalgia rates between moderate- and high-dose statins (<i>p</i> = 0.78). The proportion of myopathy was higher with simvastatin 80 mg compared to other statins. The risk of rhabdomyolysis was dose-dependent (<i>p</i> &lt; 0.01). For heart failure patients, elderly patients showed varying risks of CK elevation, gastrointestinal symptoms, and muscle symptoms (<i>I</i>² = 71<i>%</i>, 99%, and 99%, respectively). For patients with acute coronary syndrome or acute stroke, the rates of transaminase elevation were higher with simvastatin 40 mg and atorvastatin 80 mg compared to other statins (<i>p</i> &lt; 0.01). There is no difference in myalgia rates between rosuvastatin 20 mg and atorvastatin 80 mg (<i>p</i> = 0.20). However, the rate of myalgia with atorvastatin 80 mg was higher than that of rosuvastatin 10 mg and atorvastatin 20 mg (<i>p</i> &lt; 0.01). For diabetic patients, there was no difference in the effect on transaminases among four statin medications: rosuvastatin 10 and 40 mg, simvastatin 40 mg, and atorvastatin 80 mg (0.00058, 95% CI [0.00000, 0.00464], <i>I</i>² = 0<i>%</i>). Additionally, there was no difference in the rates of myalgia among atorvastatin 10, 40, and 80 mg and rosuvastatin 20 and 40 mg (<i>p</i> = 0.05).</p><p><b>Conclusion:</b> Statins’ adverse reactions differ across populations. For t","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/6684099","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244642","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":"Exploring the Mechanism of Action of Berberine on Arrhythmia After Myocardial Infarction: A Network Pharmacology, Molecular Docking, and Cellular Experimental Study","authors":"Haitian-Li,&nbsp; Zhijie-Zhang,&nbsp; Yang-Yang,&nbsp; Xiaohan-Yu,&nbsp; Jinmao-Li,&nbsp; Hongsheng-Cui,&nbsp; Ping-Li,&nbsp; Buxing-Chen","doi":"10.1155/cdr/5632985","DOIUrl":"https://doi.org/10.1155/cdr/5632985","url":null,"abstract":"<p><b>Background:</b> Arrhythmia after myocardial infarction, a common disease, has a high incidence and lethality in clinical practice, which seriously affects patients’ quality of life and survival time. Based on our previous study and available evidence, berberine plays a role in the treatment and prevention of arrhythmia after myocardial infarction. Thus, in order to clarify the specific mechanism and provide new clinical treatments, we conducted this study.</p><p><b>Method:</b> Firstly, we used bioinformatics analysis and system pharmacology to analyze the physicochemical properties and biological activities of berberine in the Molinspiration server. Secondly, we explored the potential molecular mechanism of arrhythmia after myocardial infarction treated with berberine by using network pharmacology technology: (1) obtaining common genes among berberine, myocardial infarction, and arrhythmia through TCMSP, TTD databases, and so forth; (2) constructing protein–protein interaction by using STRING database; (3) using g:Profiler database to conduct GO enrichment analysis of hub genes and pathways; and (4) performing molecular docking and visualization by using AutoDock and Pymol software. Finally, we applied Western blotting analysis and real-time quantitative polymerase chain reaction to validate the expression of relevant proteins in the TGF-<i>β</i>1-induced cell models.</p><p><b>Results:</b> The results of bioinformatics analysis and system pharmacology of berberine indicated that it had wonderful bioavailability and high biological activities. The results of network pharmacology showed that (1) 70 genes related to berberine against arrhythmia after myocardial infarction were obtained, (2) 31 hub genes were obtained by constructing PPI network, and (3) GO enrichment analysis showed that hub genes were associated with mechanisms such as stimulus and cell death. The analysis of KEGG pathways, Wiki pathways, and Reactome pathways showed that the HIF-1 signaling pathway and interleukin-4 and interleukin-13 signaling pathways were the most likely to exert therapeutic effects. (4) The results of molecular docking indicated that berberine most likely exerted therapeutic effects through acting on NGF. Western blotting analysis and real-time quantitative polymerase chain reaction techniques showed that berberine could reduce the expression of NGF and <i>α</i>-SMA in TGF-<i>β</i>1-induced cell models, which confirmed the accuracy of the above findings.</p><p><b>Conclusion:</b> Berberine can reduce NGF secretion not only by inhibiting the conversion of cardiac fibroblasts to myofibroblasts but also by acting directly on myofibroblasts. Thus, the sympathetic nerve remodeling was inhibited, which can reduce the occurrence of arrhythmia after myocardial infarction. Considering its wonderful bioavailability and high biological activities, we believe that berberine can be a novel potential therapeutic agent with potential for the treatment of arrhythmia afte","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/5632985","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144191002","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 Vasopressin on 90-Day Mortality in Patients With Cardiogenic Shock: A Retrospective Cohort Study Using Propensity Score-Weighted Analysis","authors":"Christophe Beyls,&nbsp;Thomas Hanquiez,&nbsp;Nicolas Mollet,&nbsp;Yoni Sarfati,&nbsp;Adel Zerima,&nbsp;Souheil Chafiki,&nbsp;Patricia Besserve,&nbsp;Hervé Dupont,&nbsp;Momar Diouf,&nbsp;Osama Abou-Arab,&nbsp;Yazine Mahjoub","doi":"10.1155/cdr/9920490","DOIUrl":"https://doi.org/10.1155/cdr/9920490","url":null,"abstract":"<p><b>Background:</b> Cardiogenic shock (CS) may lead to a refractory vasoplegic state that requires vasopressin on top of norepinephrine. Vasopressin has been available in France since January 2022. However, data assessing the clinical impact of vasopressin in CS are very scarce.</p><p><b>Objective:</b> In this study, we aimed to assess the association between vasopressin and 90-day mortality in a cohort of CS.</p><p><b>Method:</b> We conducted a retrospective, single-center study at Amiens University Hospital comparing two cohorts of patients experiencing at least Stage C of CS: one historical cohort from 2018 to 2019 without vasopressin and a contemporary cohort from 2022 to 2023 treated with vasopressin. The primary outcome was 90-day mortality. The secondary outcome was the occurrence of serious adverse events (SAEs) during ICU stay. Inverse probability of treatment weighting (IPTW) derived from propensity score was used to reduce imbalances in baseline characteristics.</p><p><b>Results:</b> We included 201 patients in the study: 59 in the vasopressin group and 142 in the no vasopressin group. The SOFA score and norepinephrine equivalent were higher in the vasopressin group (13 [10–16] vs. 12 [9–15]; <i>p</i> = 0.02 and 0.72 [0.21–1.51] vs. 0.13 [0.07–0.34]; <i>p</i> &lt; 0.001, respectively). There was no significant difference between the two groups for the 90-day mortality (<i>n</i> = 31/59 vs. 75/142; <i>p</i> = 0.97). Before adjustment, vasopressin was not associated with 90-day mortality (OR = 0.98 [95% CI 0.50–1.78]; <i>p</i> = 0.87). After weighting, vasopressin remained not associated with 90-day mortality (OR = 1.10 [95% CI 0.56–2.17]; <i>p</i> = 0.77). There was no significant difference for SAEs between the two groups (<i>n</i> = 57/142 [40%] vs. <i>n</i> = 23/59 [39%]; <i>p</i> = 0.88).</p><p><b>Conclusion:</b> Vasopressin was not associated with 30-day mortality and SAEs in patients with CS.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/9920490","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144148384","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":"Characteristics of Cardiac Ketone Body Metabolism Throughout the Life Cycle","authors":"Lei Li,&nbsp;Xiaojian Song,&nbsp;Xiurui Ma,&nbsp;Yanwu Xu","doi":"10.1155/cdr/5913327","DOIUrl":"https://doi.org/10.1155/cdr/5913327","url":null,"abstract":"<p>Ketone bodies can serve as energy substrates for the heart and perform important molecular signal transduction functions. In recent years, the therapeutic potential of ketone bodies has become a research hotspot in the field of cardiovascular diseases. Many previous reviews have focused on ketone bodies from the perspective of cardiovascular diseases, especially heart failure. Nonetheless, the metabolism of cardiac ketone bodies under physiological conditions also warrants attention, as the consumption of a ketogenic diet or direct supplementation of ketone bodies from exogenous sources has become widely popular among healthy individuals for weight loss. Furthermore, recent clinical studies have shown that under physiological conditions, the level of ketone bodies is positively correlated with the incidence of cardiovascular diseases and mortality. On the basis of the differences in cardiac ketone body metabolism under healthy and disease conditions, in this review, we describe in detail the characteristics of cardiac ketone body metabolism and the significance of elevated circulating ketone body levels throughout the life cycle on physiological states.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/5913327","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144135866","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":"FBXO38 Regulates Nox1 Stability to Reduce Vascular Endothelial Damage Induced by Low Oscillatory Shear Stress","authors":"Wan-li Yu,&nbsp;Li-wen Deng,&nbsp;Huan-huan Li,&nbsp;Chun-kai Wang,&nbsp;Xiang-yi Zuo,&nbsp;Zi-chang Wang,&nbsp;Li Meng,&nbsp;Lan-xin Wen,&nbsp;Wan-zhi Zeng,&nbsp;Yu Zhao,&nbsp;Xue-hu Wang","doi":"10.1155/cdr/4506032","DOIUrl":"https://doi.org/10.1155/cdr/4506032","url":null,"abstract":"<p>Oxidative stress and endothelial dysfunction are critical drivers of atherosclerosis, but the mechanisms regulating oxidative stress under disturbed flow conditions remain incompletely understood. The ubiquitin–proteasome system, particularly E3 ubiquitin ligases, may play a pivotal role in modulating these processes. FBXO38, an E3 ligase involved in proteasomal degradation, has been implicated in various physiological pathways, but its role in regulating oxidative stress in endothelial cells is unknown. We hypothesized that FBXO38 mitigates endothelial damage induced by low oscillatory shear stress (LOSS) by promoting the ubiquitin–proteasome–dependent degradation of Nox1, a major source of reactive oxygen species (ROS). Using an in vitro LOSS model in human umbilical vein endothelial cells (HUVECs) and an in vivo mouse partial carotid ligation model, we assessed the expression of FBXO38 and Nox1 through quantitative PCR, western blotting, immunofluorescence, and immunohistochemistry. LOSS significantly reduced FBXO38 protein expression (by ~60%, <i>p</i> &lt; 0.0001 at 24 h), leading to increased Nox1 protein levels (approximately two-fold, <i>p</i> &lt; 0.001) and apoptosis. FBXO38 overexpression markedly attenuated Nox1 accumulation (~50% reduction, <i>p</i> &lt; 0.05), reduced ROS production, and improved cell viability under LOSS conditions, whereas FBXO38 knockdown exacerbated these effects. Moreover, FBXO38 directly interacted with Nox1, suggesting a ubiquitin-dependent degradation mechanism. Our results reveal that FBXO38 regulates endothelial oxidative stress by controlling Nox1 stability under disturbed shear stress conditions. Although FBXO38 emerges as a promising candidate for therapeutic targeting, further studies are necessary to validate its potential in preclinical and clinical settings.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/4506032","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143861897","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":"Metabolic Profiling Reveals Diagnostic Biomarkers for Distinguishing Myocarditis From Acute Myocardial Infarction","authors":"Yuting Chen,&nbsp;Xiu Liu,&nbsp;Chengying Hong,&nbsp;Shunyao Xu,&nbsp;Linling He,&nbsp;Zhenmi Liu,&nbsp;Huaisheng Chen,&nbsp;Yaowang Lin","doi":"10.1155/cdr/6292099","DOIUrl":"https://doi.org/10.1155/cdr/6292099","url":null,"abstract":"<p><b>Background:</b> Distinguishing between myocarditis (MC) and acute myocardial infarction (AMI) in the early stages is crucial due to their similar symptoms yet vastly different treatment protocols. This study seeks to utilize metabolomics techniques to differentiate between MC and AMI.</p><p><b>Methods:</b> Plasma samples from 15 patients with MC and 12 patients with AMI were collected. Metabolic profiles of plasma from the two groups of patients were obtained using ultra-high performance liquid chromatography–mass spectrometry (UHPLC-MS), identifying metabolites with significant differences.</p><p><b>Results:</b> We identified 30 significantly different metabolites in both diseases. In patients with MC, 17 metabolites were upregulated, including 5-hydroxy-L-tryptophan and LysoPC (18:2(9Z,12Z)), while 13 metabolites were downregulated, such as 11-<i>cis</i>-retinol, L-glutamate, and hydroxynicotinic acid. KEGG enrichment analysis revealed that the altered metabolites were enriched in tryptophan metabolism, linoleic acid metabolism, primary bile acid biosynthesis, nitrogen metabolism, and retinol metabolism. Biomarker analysis via receiver-operating characteristic curves highlighted 11-<i>cis</i>-retinol as the predominant biomarker, with an AUC value of 0.917.</p><p><b>Conclusions:</b> In conclusion, patients experiencing AMI and MC undergo significant metabolic reprogramming. Metabolites exhibiting abnormal expression in peripheral blood hold diagnostic value for distinguishing between AMI and MC in clinical settings. 11-<i>cis</i>-retinol proved to be the pivotal biomarker for AMI, potentially aiding in the development of a robust predictive model for distinguishing between MC and AMI in clinical settings.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/6292099","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836125","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":"Does Spontaneous Echo Contrast in the Left Atrial Appendage Increase Thromboembolism Risk After Left Atrial Appendage Closure? A Retrospective Study on Its Impact on Device-Related Thrombosis and Arterial Thromboembolic Events","authors":"Kandi Zhang,&nbsp;Hanwen Yu,&nbsp;Yihua Lu,&nbsp;Peng Zhang,&nbsp;Dongsheng Liu,&nbsp;Jianpeng Huang,&nbsp;Jing Zhou,&nbsp;Yiqian Yuan,&nbsp;Zongqi Zhang,&nbsp;Qingyong Zhang,&nbsp;Qing He,&nbsp;Junfeng Zhang","doi":"10.1155/cdr/1849432","DOIUrl":"https://doi.org/10.1155/cdr/1849432","url":null,"abstract":"<p><b>Background:</b> Left atrial appendage closure (LAAC) prevents arterial thromboembolic events (ATEs) in nonvalvular atrial fibrillation (AF). Spontaneous echo contrast (SEC) is an independent risk factor for left atrial appendage (LAA) thrombosis; however, there is little knowledge about the relationship between preoperative SEC and the increased risk of device-related thrombosis (DRT) or ATEs in patients with AF who have undergone LAAC.</p><p><b>Methods:</b> This retrospective study focused on patients with nonvalvular AF who successfully underwent LAAC surgery. Transesophageal echocardiography (TEE) was used to assess preoperative LAA status. SEC in LAA Grades 0–2 was defined as LAASEC−, and Grades 3–4 or previously diagnosed LAA thrombus formation as LAASEC+.</p><p><b>Results:</b> A total of 519 AF patients (432 in LAASEC− group and 87 in LAASEC+ group) who underwent LAAC were included. At the 1-year follow-up, there was no significant difference in the incidence of DRT (2.5 vs. 3.8%, <i>p</i> = 0.636), ATEs (0.5 vs. 0%, <i>p</i> = 0.525), and all-cause mortality (2.1% vs. 2.3%, <i>p</i> = 0.899) between the LAASEC− group and the LAASEC+ group. However, the LAASEC+ group had higher proportions of cauliflower-type LAA and ≥ 3 lobes.</p><p><b>Conclusions:</b> The difference in preoperative LAA thrombosis or LAASEC was not related to the incidence of DRT or ATEs in AF patients within 1 year after LAAC.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/1849432","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143818531","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}