Vascular pharmacology最新文献_第2页

Endostatin in disease modulation: From cancer to beyond 内皮抑素在疾病调节中的作用：从癌症到其他疾病。

IF 3.5 3区医学

Vascular pharmacology Pub Date : 2024-12-19 DOI: 10.1016/j.vph.2024.107459

J. Anakha, Yenisetti Rajendra Prasad, Abhay H. Pande

引用次数: 0

Targeting the Ca2+ signaling toolkit as an alternative strategy to mitigate SARS-CoV-2-induced cardiovascular adverse events 靶向Ca2+信号工具箱作为缓解sars - cov -2诱导的心血管不良事件的替代策略

IF 3.5 3区医学

Vascular pharmacology Pub Date : 2024-12-17 DOI: 10.1016/j.vph.2024.107458

Simona Scorza , Valentina Brunetti , Giorgia Scarpellino , Maira Certini , Andrea Gerbino , Francesco Moccia

{"title":"Targeting the Ca2+ signaling toolkit as an alternative strategy to mitigate SARS-CoV-2-induced cardiovascular adverse events","authors":"Simona Scorza , Valentina Brunetti , Giorgia Scarpellino , Maira Certini , Andrea Gerbino , Francesco Moccia","doi":"10.1016/j.vph.2024.107458","DOIUrl":"10.1016/j.vph.2024.107458","url":null,"abstract":"<div><div>Ca<sup>2+</sup> signaling events are essential for maintaining cardiovascular health, regulating critical functions in both endothelial and cardiac cells. SARS-CoV-2 infection impinges this delicate balance, leading to severe cardiovascular complications. SARS-CoV-2 binds to the ACE2 receptor on endothelial and cardiomyocyte surfaces, triggering abnormal increases in intracellular Ca<sup>2+</sup> levels that promote endothelial dysfunction, inflammation, and hypercoagulation. In endothelial cells, this dysregulation activates a pro-inflammatory state and compromises vascular integrity. In cardiomyocytes, SARS-CoV-2-induced Ca<sup>2+</sup> imbalances contribute to arrhythmias and heart failure by promoting abnormal Ca<sup>2+</sup> cycling and energy metabolism disruptions. Additionally, the cytokine storm associated with COVID-19 amplifies these effects by further altering Ca<sup>2+</sup> handling, enhancing inflammatory responses, and promoting thrombosis. Targeting Ca<sup>2+</sup> channels, particularly endolysosomal two-pore channels, represents a promising therapeutic approach to counteract SARS-CoV-2’s effects on Ca<sup>2+</sup> dynamics. Several FDA-approved drugs that modulate Ca<sup>2+</sup> signaling could be repurposed to prevent viral entry and mitigate cardiovascular damage. Understanding these Ca<sup>2+</sup>-related mechanisms offers valuable insights for developing treatments to reduce cardiovascular risk in COVID-19 and potentially future viral infections impacting the cardiovascular system.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107458"},"PeriodicalIF":3.5,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142865441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of Epsins in atherosclerosis: From molecular mechanisms to therapeutic applications epsin在动脉粥样硬化中的作用：从分子机制到治疗应用。

IF 3.5 3区医学

Vascular pharmacology Pub Date : 2024-12-11 DOI: 10.1016/j.vph.2024.107457

Siarhei A. Dabravolski , Alexey V. Churov , Alessio L. Ravani , Amina E. Karimova , Igor G. Luchinkin , Vasily N. Sukhorukov , Alexander N. Orekhov

{"title":"The role of Epsins in atherosclerosis: From molecular mechanisms to therapeutic applications","authors":"Siarhei A. Dabravolski , Alexey V. Churov , Alessio L. Ravani , Amina E. Karimova , Igor G. Luchinkin , Vasily N. Sukhorukov , Alexander N. Orekhov","doi":"10.1016/j.vph.2024.107457","DOIUrl":"10.1016/j.vph.2024.107457","url":null,"abstract":"<div><div>Atherosclerosis is a multifaceted disease characterised by chronic inflammation and vascular remodelling, leading to plaque formation and cardiovascular complications. Recent evidence highlights the critical role of epsins, a family of endocytic proteins, in the pathogenesis of atherosclerosis. This manuscript explores the multifarious functions of epsins in atherosclerosis, focusing on their involvement in angiogenesis, lymphangiogenesis, and the modulation of key signalling pathways. We discuss how epsins facilitate EndoMT through their interaction with the TGFβ signalling pathway, which contributes to vascular smooth muscle cell-like phenotypes and plaque instability. Additionally, we examine the therapeutic potential of targeting epsins, elucidating their interactions with crucial partners such as LDLR, LRP-1, and TLR 2/4, among others, in mediating lipid metabolism and inflammation. Furthermore, we highlight the promising prospects of epsin-targeting peptides and small interfering RNAs as therapeutic agents for atherosclerosis treatment. Despite these advancements, the research faces limitations, including a reliance on specific mouse models and a need for comprehensive studies on the long-term effects of epsin modulation. Therefore, future investigations should focus on elucidating the detailed mechanisms of epsin function and their implications in cardiovascular health, fostering collaborations to translate basic research into innovative therapeutic strategies. This work underscores the necessity for further exploration of epsins to unlock their full therapeutic potential in combating atherosclerosis and related cardiovascular diseases.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107457"},"PeriodicalIF":3.5,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142822174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Unravelling molecular mechanisms in atherosclerosis using cellular models and omics technologies 利用细胞模型和 omics 技术揭示动脉粥样硬化的分子机制。

IF 3.5 3区医学

Vascular pharmacology Pub Date : 2024-12-10 DOI: 10.1016/j.vph.2024.107452

Dimitris Kardassis , Cécile Vindis , Camelia Sorina Stancu , Laura Toma , Anca Violeta Gafencu , Adriana Georgescu , Nicoleta Alexandru-Moise , Filippo Molica , Brenda R. Kwak , Alexandrina Burlacu , Ignacio Fernando Hall , Elena Butoi , Paolo Magni , Junxi Wu , Susana Novella , Luke F. Gamon , Michael J. Davies , Andrea Caporali , Fernando de la Cuesta , Tijana Mitić

{"title":"Unravelling molecular mechanisms in atherosclerosis using cellular models and omics technologies","authors":"Dimitris Kardassis , Cécile Vindis , Camelia Sorina Stancu , Laura Toma , Anca Violeta Gafencu , Adriana Georgescu , Nicoleta Alexandru-Moise , Filippo Molica , Brenda R. Kwak , Alexandrina Burlacu , Ignacio Fernando Hall , Elena Butoi , Paolo Magni , Junxi Wu , Susana Novella , Luke F. Gamon , Michael J. Davies , Andrea Caporali , Fernando de la Cuesta , Tijana Mitić","doi":"10.1016/j.vph.2024.107452","DOIUrl":"10.1016/j.vph.2024.107452","url":null,"abstract":"<div><div>Despite the discovery and prevalent clinical use of potent lipid-lowering therapies, including statins and PCSK9 inhibitors, cardiovascular diseases (CVD) caused by atherosclerosis remain a large unmet clinical need, accounting for frequent deaths worldwide. The pathogenesis of atherosclerosis is a complex process underlying the presence of modifiable and non-modifiable risk factors affecting several cell types including endothelial cells (ECs), monocytes/macrophages, smooth muscle cells (SMCs) and T cells. Heterogeneous composition of the plaque and its morphology could lead to rupture or erosion causing thrombosis, even a sudden death. To decipher this complexity, various cell model systems have been developed. With recent advances in systems biology approaches and single or multi-omics methods researchers can elucidate specific cell types, molecules and signalling pathways contributing to certain stages of disease progression. Compared with animals, <em>in vitro</em> models are economical, easily adjusted for high-throughput work, offering mechanistic insights. Hereby, we review the latest work performed employing the cellular models of atherosclerosis to generate a variety of omics data. We summarize their outputs and the impact they had in the field. Challenges in the translatability of the omics data obtained from the cell models will be discussed along with future perspectives.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107452"},"PeriodicalIF":3.5,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Prevalence of antiphospholipid antibodies in COVID-19 patients: A meta-analysis COVID-19患者抗磷脂抗体患病率：一项荟萃分析

IF 3.5 3区医学

Vascular pharmacology Pub Date : 2024-12-03 DOI: 10.1016/j.vph.2024.107444

Er Jin , Bei Li , Xiaonan Wang , Runlan Yan , Chenhong Yan , Yue Gao

{"title":"Prevalence of antiphospholipid antibodies in COVID-19 patients: A meta-analysis","authors":"Er Jin , Bei Li , Xiaonan Wang , Runlan Yan , Chenhong Yan , Yue Gao","doi":"10.1016/j.vph.2024.107444","DOIUrl":"10.1016/j.vph.2024.107444","url":null,"abstract":"<div><h3>Objective</h3><div>In some reports, antiphospholipid antibodies (aPL) prevalence is higher in COVID-19 patients. This study intended to compare aPL prevalence between COVID-19 patients and healthy controls, and differences in aPL types using meta-analysis.</div></div><div><h3>Methods</h3><div>This work retrieved published literature about association between COVID-19 and aPL from Embase, Web of Science, PubMed, and The Cochrane Library databases. The observation group was COVID-19 patients, and the control group was healthy individuals. Outcome measures contained any of following aPLs: classic aPL: anti-cardiolipin antibodies (aCL) and anti-β2-glycoprotein-1 antibodies (Anti-β2GP1); other non-criteria aPL: anti-phosphatidylserine/prothrombin antibodies (aPS/PT) and anti-annexin-V antibodies (AnV). Meta-analysis was done on Review Manager 5.4.</div></div><div><h3>Results</h3><div>10 studies involving 2288 patients were deemed eligible for inclusion. The results of the meta-analysis showed that the prevalence of Classic aPL and Any aPL in the COVID-19 group was significantly higher than in the healthy group (Classic aPL, RR = 2.55, 95 % CI = 1.83–3.55, <em>P</em> < 0.00001; Any aPL, RR = 2.34, 95 % CI = 1.46–3.77, <em>P</em> = 0.0005). Anti-β2GP1 IgA antibodies were the most common aPL in COVID-19 patients, with a significantly higher prevalence than in the healthy group (RR = 4.26, 95 % CI = 2.84–6.40, <em>P</em> < 0.00001). The prevalence of the four types of IgM aPL was significantly higher in the COVID-19 group compared to the healthy group, while there was no significant difference in aPL IgG between the two groups.</div></div><div><h3>Conclusion</h3><div>The prevalence of aPL in COVID-19 patients was significantly higher than in the healthy control group. IgM aPL was more easily detectable in the early stages of COVID-19 infection, while IgG aPL may be of more concern in the later time points of the immune epidemiology following SARS-CoV-2 infection.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107444"},"PeriodicalIF":3.5,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142787324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Patterns of medication use and potential drug-drug interactions in post-PCI patients: A study from Iran 重症介入治疗后患者的用药模式和潜在的药物相互作用：伊朗的一项研究。

IF 3.5 3区医学

Vascular pharmacology Pub Date : 2024-12-01 DOI: 10.1016/j.vph.2024.107441

Reza Golchin Vafa , Hossein Molavi Vardanjani , Javad Kojuri

{"title":"Patterns of medication use and potential drug-drug interactions in post-PCI patients: A study from Iran","authors":"Reza Golchin Vafa , Hossein Molavi Vardanjani , Javad Kojuri","doi":"10.1016/j.vph.2024.107441","DOIUrl":"10.1016/j.vph.2024.107441","url":null,"abstract":"<div><h3>Background</h3><div>Post-percutaneous coronary intervention (PCI) patients often require complex medication regimens to prevent adverse cardiovascular events. However, these regimens can lead to potential drug-drug interactions (pDDIs) and polypharmacy, posing significant clinical challenges. This study aims to evaluate the pattern of medication use, prevalence, and correlates of pDDIs and polypharmacy among post-PCI patients in Shiraz, Iran.</div></div><div><h3>Methods</h3><div>A cross-sectional study was conducted on 9019 PCI patients in Shiraz. Patient data, including demographics, medical history, and medication lists, were collected and analyzed. The Anatomical Therapeutic Chemical (ATC) classification system was applied. pDDIs were identified using the Lexicomp database, and their severity was classified. Factors associated with significant pDDIs and polypharmacy were assessed using multivariable modeling.</div></div><div><h3>Results</h3><div>The study found that 91.6 % of patients received statin prescriptions and 94.5 % were on antiplatelet therapy. Notably, 82.8 % were identified with at least one pDDI, with 80.4 % having significant interactions (Categories C, D, or X). Common potential interactions included aspirin with clopidogrel and rosuvastatin. Polypharmacy was prevalent in 73.6 % of patients, associated with higher risks of interactions. Factors such as polypharmacy, male gender, diabetes mellitus, and heart failure were significant predictors of pDDIs.</div></div><div><h3>Conclusions</h3><div>The study underscores the high prevalence of pDDIs and polypharmacy among post-PCI patients, revealing a critical gap between clinical guidelines and drug interaction databases. Updating interaction databases to reflect current clinical practices and enhancing collaboration between database developers and guideline authors are essential for improving medication safety and patient outcomes.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"157 ","pages":"Article 107441"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142710830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

New insights into the pharmacological inhibition of SRF activity: Key inhibitory targets and mechanisms 药理抑制 SRF 活性的新见解：关键抑制靶点和机制

IF 3.5 3区医学

Vascular pharmacology Pub Date : 2024-12-01 DOI: 10.1016/j.vph.2024.107443

Daniel Wong , Hongyu Qiu

引用次数: 0

Sotatercept: New drug on the horizon of pulmonary hypertension 索泰特受体：肺动脉高压领域的新药。

IF 3.5 3区医学

Vascular pharmacology Pub Date : 2024-11-19 DOI: 10.1016/j.vph.2024.107442

Rosalinda Madonna, Filippo Biondi

引用次数: 0

LncRNA MYOSLID contributes to PH via targeting BMPR2 signaling in pulmonary artery smooth muscle cell LncRNA MYOSLID通过靶向肺动脉平滑肌细胞中的BMPR2信号对PH做出了贡献。

IF 3.5 3区医学

Vascular pharmacology Pub Date : 2024-11-15 DOI: 10.1016/j.vph.2024.107439

Yuan Chen , Yuan Li , Bin Leng , Chengrui Cao , Guifu Wu , Shugao Ye , Lin Deng

{"title":"LncRNA MYOSLID contributes to PH via targeting BMPR2 signaling in pulmonary artery smooth muscle cell","authors":"Yuan Chen , Yuan Li , Bin Leng , Chengrui Cao , Guifu Wu , Shugao Ye , Lin Deng","doi":"10.1016/j.vph.2024.107439","DOIUrl":"10.1016/j.vph.2024.107439","url":null,"abstract":"<div><h3>Background/objective</h3><div>The pathogenesis and vascular remodeling during pulmonary hypertension (PH) have been associated with dysregulation of bone morphogenetic protein receptor type 2 (BMPR2) and transforming growth factor-β (TGF-β) signaling in pulmonary artery smooth muscle cells (PASMCs). Evidence suggests that the human-specific lncRNA <em>MYOSLID</em> is a transcriptional target of the TGF-β/SMAD pathway. In this study, we investigated the involvement of <em>MYOSLID</em> in the pathogenesis of PH.</div></div><div><h3>Methods</h3><div>Lung tissues from PH patients and rat PH models were analyzed to assess clinical relevance. RNA-Seq was performed to identify target genes. Pulmonary artery smooth muscle cells (PASMCs) were used to evaluate function and underlying mechanisms.</div></div><div><h3>Results</h3><div>RNA-Seq analysis of PASMCs stimulated by TGF-β1 revealed significantly dysregulated lncRNAs. <em>MYOSLID</em> expression was markedly elevated in lung tissues from PH patients and in PASMCs stimulated with TGF-β1. Mechanistically, loss of <em>MYOSLID</em> inhibited the TGF-β pathway by reducing SMAD2/3 PHosphorylation and activated the BMPR2 pathway by enhancing SMAD1/5/9 phosphorylation and increasing ID genes expression in PASMCs. DAZAP2, a target gene of <em>MYOSLID</em>, functions as an inhibitor of BMPR2 signaling. Moreover, DAZAP2 expression was significantly elevated in lung tissues from PH patients and rat PH models. Functionally, knockdown of <em>MYOSLID</em> and DAZAP2 reduced proliferation, migration, and apoptosis resistance in PASMCs.</div></div><div><h3>Conclusion</h3><div>The activation of the <em>MYOSLID</em>-DAZAP2-BMPR2 axis contributes to pulmonary vascular remodeling, and targeting <em>MYOSLID</em> and DAZAP2 may represent novel therapeutic strategies for PH treatment.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"157 ","pages":"Article 107439"},"PeriodicalIF":3.5,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142645052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Prolonged L-NAME exposure changes the vasodilator factor from NO to H2O2 in human arterioles in response to A23187 长期暴露于 L-NAME 会使人体动脉血管中的血管扩张因子从 NO 转变为 H2O2，从而对 A23187 产生反应。

IF 3.5 3区医学

Vascular pharmacology Pub Date : 2024-11-12 DOI: 10.1016/j.vph.2024.107440

Natalya S. Zinkevich , Kostiantyn Drachuk , David X. Zhang

{"title":"Prolonged L-NAME exposure changes the vasodilator factor from NO to H2O2 in human arterioles in response to A23187","authors":"Natalya S. Zinkevich , Kostiantyn Drachuk , David X. Zhang","doi":"10.1016/j.vph.2024.107440","DOIUrl":"10.1016/j.vph.2024.107440","url":null,"abstract":"<div><div>The Ca<sup>2+</sup> ionophore A23187 induces endothelium-dependent and non-receptor-mediated vasodilation in human adipose arterioles (HAAs). The purpose of this study was to determine the mechanism of A23187-induced dilation in HAAs from patients with and without coronary artery disease (CAD). HAAs were freshly isolated from adipose tissues obtained from non-CAD (<em>n</em> = 25) and CAD (<em>n</em> = 14) patients, and vascular reactivity was studied by videomicroscopy. No difference in baseline dose response to A23187 was observed between non-CAD and CAD subjects. However, acute (30 min) incubation with N(omega)-nitro-l-arginine methyl ester (L-NAME), NO synthase inhibitor strongly reduced A23187-induced dilation in non-CAD arterioles, while catalase, an H<sub>2</sub>O<sub>2</sub> scavenger, largely abolished dilation in CAD. Surprising, prolonged (90 min) incubation with L-NAME restored A23187 response in non-CAD subjects, which was subsequently inhibited by catalase. The action of prolonged L-NAME exposure was not reversible after washing with Krebs while the effect of acute L-NAME exposure was largely reversible. To further determine the role of mitochondria-derived ROS in A23187-induced dilation, arterioles were treated with rotenone, an inhibitor of complex I of the electron transport chain. Rotenone abolished A23187 response in CAD patients and in non-CAD arterioles after prolonged L-NAME, but not in non-CAD controls. These data indicate that NO contributes to A23187-induced dilation in HAAs from non-CAD patients and H<sub>2</sub>O<sub>2</sub> contributes to the dilation in CAD patients. Prolonged L-NAME exposure induces a NO-H<sub>2</sub>O<sub>2</sub> switch in the mechanism of dilation in non-CAD subjects. Moreover, the effect of prolonged L-NAME exposure is not readily reversible, while the action of acute L-NAME exposure is reversible.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"157 ","pages":"Article 107440"},"PeriodicalIF":3.5,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142629271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0