Vascular pharmacology最新文献

{"title":"TNAP expressing adventitial pericytes contribute to myogenesis during foetal development","authors":"I. Fancello ,&nbsp;S. Willett ,&nbsp;C. Castiglioni ,&nbsp;S. Amer ,&nbsp;S. Santoleri ,&nbsp;L. Bragg ,&nbsp;F. Galli ,&nbsp;G. Cossu","doi":"10.1016/j.vph.2025.107489","DOIUrl":"10.1016/j.vph.2025.107489","url":null,"abstract":"<div><h3>Objective</h3><div>During growth and differentiation of skeletal muscle, cell types other than canonical myoblasts can be recruited to a myogenic fate. Among these, TNAP+ pericytes can differentiate into skeletal or smooth muscle cells during postnatal growth and contribute to muscle regeneration. However, their role in muscle development has not been investigated. This study aims to characterise pericyte fate choices during embryonic and foetal myogenesis, occurring in the second half of gestation.</div></div><div><h3>Approach and results</h3><div>Using Cre-loxP lineage tracing with multiple reporters including the multifluorescent Confetti, we labelled TNAP+ precursors <em>in vivo</em> and assessed the smooth or skeletal muscle differentiation in their lineage at a perinatal stage. We found that TNAP+ cells contribute <em>in vivo</em> to skeletal and smooth muscle cells, as well as other pericytes, also during pre-natal muscle development. The resulting clones showed that such fate choices are likely to depend on distinct unipotent progenitors rather than multipotent progenitors. In addition, we isolated and differentiated <em>in vitro</em> foetal cells derived from TNAP+ precursors, which showed that they are not spontaneously myogenic unless co-cultured with other skeletal muscle cells.</div></div><div><h3>Conclusions</h3><div>This work extends our understanding of the differentiative potency of these non- canonical skeletal muscle progenitors during prenatal life, with a view to a future application of this knowledge to optimise cell therapies for muscle wasting disorders.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107489"},"PeriodicalIF":3.5,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143651057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Non-coding RNAs regulate angiogenic processes” [Vascular pharmacology 133–134 (2020) 106778]","authors":"Soudeh Ghafouri-Fard ,&nbsp;Hamed Shoorei ,&nbsp;Mahdi Mohaqiq ,&nbsp;Mohammad Taheri","doi":"10.1016/j.vph.2025.107486","DOIUrl":"10.1016/j.vph.2025.107486","url":null,"abstract":"","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107486"},"PeriodicalIF":3.5,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143562157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interspecies differences in mitochondria: Implications for cardiac and vascular translational research","authors":"Lisa Alibrandi ,&nbsp;Vincenzo Lionetti","doi":"10.1016/j.vph.2025.107476","DOIUrl":"10.1016/j.vph.2025.107476","url":null,"abstract":"<div><div>Mitochondria are essential organelles that regulate cellular energy metabolism, redox balance, and signaling pathways related to proliferation, aging and survival. So far, significant interspecies differences exist in mitochondrial structure, function, and dynamics, which have critical implications for cardiovascular physiology and pharmacology. This review explores the main differences in mitochondrial properties across species of animals that are commonly used for translational research, emphasizing their cardiac and vascular relevance. By addressing key interspecies differences, including mitochondrial DNA (mtDNA) variation, bioenergetic profile, oxidative stress response, epigenetic regulation, mitochondrial biogenesis, and adaptive mechanisms, we aim to provide insights into the challenges and opportunities in translating preclinical findings to clinical applications. Understanding these interspecies differences is essential for optimizing the design and interpretation of preclinical studies and for developing effective mitochondrial-targeted therapies.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107476"},"PeriodicalIF":3.5,"publicationDate":"2025-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143558223","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}

{"title":"Survivin in cardiovascular diseases and its therapeutic potential","authors":"Thomas Mousso ,&nbsp;Khanh Pham ,&nbsp;Rhonda Drewes ,&nbsp;Sefunmi Babatunde ,&nbsp;Jessica Jong ,&nbsp;Alanna Krug ,&nbsp;Gabrielle Inserra ,&nbsp;John Biber ,&nbsp;Joseph A. Brazzo ,&nbsp;Sachin Gupte ,&nbsp;Yongho Bae","doi":"10.1016/j.vph.2025.107475","DOIUrl":"10.1016/j.vph.2025.107475","url":null,"abstract":"<div><div>Aberrant changes in cell behaviors, such as proliferation, apoptosis, and migration, are some of the contributing factors to the development of various cardiovascular diseases (CVDs) and pathologies, including atherosclerosis, neointimal hyperplasia, and heart failure. In recent years, numerous studies have identified survivin, a key player in the anti-apoptotic pathway, to be extensively involved in modulating cellular functioning in cancer, with many reaching clinical trials. Though seemingly different, CVDs and cancer share abundant similarities regarding abnormal cell modifications and behaviors. This overlap has sparked growing interest in investigating survivin as a therapeutic target in the context of CVD. With new findings emerging rapidly, a comprehensive understanding of survivin's role in cardiovascular pathology is crucial to revealing its full therapeutic potential and translating these discoveries into effective treatments. This review discusses recent findings of survivin in CVDs and related pathologies, focusing on its dual role in promoting proliferation and inhibiting apoptosis, specifically in atherosclerosis, neointimal hyperplasia, stroke, hypertension, myocardial infarction, and heart failure. Across different cell types and pathological contexts, survivin plays a pivotal role throughout the disease progression–from the onset of disease development to the facilitation of compensatory mechanisms post-injury–primarily through its function in regulating cell proliferation and apoptosis. Furthermore, given the limited research on survivin as a therapeutic target for CVDs, potential clinical avenues, including YM155 (a survivin inhibitor) or adenoviral, adeno-associated, and lentiviral vectors, are also discussed. Overall, this review highlights survivin as a promising target for mitigating the detrimental effects of CVDs and to provide new perspectives to advance research on the intervention of CVDs and associated pathologies.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107475"},"PeriodicalIF":3.5,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143508341","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}

{"title":"Emerging role of mesenchymal cells in cardiac and cerebrovascular diseases: Physiology, pathology, and therapeutic implications","authors":"Kajal Kumari ,&nbsp;Kanika Verma ,&nbsp;Meenal Sahu ,&nbsp;Jaya Dwivedi ,&nbsp;Sarvesh Paliwal ,&nbsp;Swapnil Sharma","doi":"10.1016/j.vph.2025.107473","DOIUrl":"10.1016/j.vph.2025.107473","url":null,"abstract":"<div><div>In recent years, the therapeutic utility of mesenchymal stem cells (MSCs) has received substantial attention from investigators, owing to their pleiotropic properties. The emerging insights from the developments in tissue engineering provide perspectives for the repair of damaged tissue and the replacement of failing organs. Perivascular cells including MSC-like pericytes, vascular smooth muscles, and other cells located around blood vessels, have been acknowledged to contribute to in situ angiogenesis and repair process. MSCs offer a wide array of therapeutic applications in different pathological states. However, in the current article, we have highlighted the recent updates on MSCs and their key applications in cardiac and cerebrovascular diseases, evident in different preclinical and clinical studies. We believe the present article would assist the investigators in understanding the recent advances of MSCs and exploring their therapeutic potential in varied ailments, especially cardiac and cerebrovascular diseases.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107473"},"PeriodicalIF":3.5,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143493729","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}

{"title":"N-glycosylation signature and its relevance in cardiovascular immunometabolism","authors":"Monika Svecla ,&nbsp;Ruifang Li-Gao ,&nbsp;David Falck ,&nbsp;Fabrizia Bonacina","doi":"10.1016/j.vph.2025.107474","DOIUrl":"10.1016/j.vph.2025.107474","url":null,"abstract":"<div><div>Glycosylation is a post-translational modification in which complex, branched carbohydrates (glycans) are covalently attached to proteins or lipids. Asparagine-link protein (<em>N</em>-) glycosylation is among the most common types of glycosylation. This process is essential for many biological and cellular functions, and impaired <em>N</em>-glycosylation has been widely implicated in inflammation and cardiovascular diseases. Different technical approaches have been used to increase the coverage of the <em>N</em>-glycome, revealing a high level of complexity of glycans, regarding their structure and attachment site on a protein. In this context, new insights from genomic studies have revealed a genetic regulation of glycosylation, linking genetic variants to total plasma <em>N</em>-glycosylation and <em>N</em>-glycosylation of immunoglobulin G (IgG). In addition, RNAseq approaches have revealed a degree of transcriptional regulation for the glycoenzymes involved in glycan structure. However, our understanding of the association between cardiovascular risk and glycosylation, determined by a complex overlay of genetic and environmental factors, remains limited. Mostly, plasma <em>N</em>-glycosylation profiling in different human cohorts or experimental investigations of specific enzyme functions in models of atherosclerosis have been reported. Most of the uncovered glycosylation associations with pathological mechanisms revolve around the recruitment of inflammatory cells to the vessel wall and lipoprotein metabolism. This review aims to summarise insights from omics studies into the immune and metabolic regulation of <em>N</em>-glycosylation and its association with cardiovascular and metabolic disease risk and to provide mechanistic insights from experimental models.</div><div>The combination of emerging techniques for glycomics and glycoproteomics with already achieved omics approaches to map the transcriptomic, epigenomic, and metabolomic profile at single-cell resolution will deepen our understanding of the molecular regulation of glycosylation as well as identify novel biomarkers and targets for cardiovascular disease prevention and treatment.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107474"},"PeriodicalIF":3.5,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143484156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cdc42 is crucial for mural cell migration, proliferation and patterning of the retinal vasculature","authors":"Alberto Álvarez-Aznar ,&nbsp;Malavika Desai ,&nbsp;Michael M. Orlich ,&nbsp;Elisa Vázquez-Liébanas ,&nbsp;Ralf H. Adams ,&nbsp;Cord Brakebusch ,&nbsp;Konstantin Gaengel","doi":"10.1016/j.vph.2025.107472","DOIUrl":"10.1016/j.vph.2025.107472","url":null,"abstract":"<div><h3>Aims</h3><div>Mural cells constitute the outer lining of blood vessels and are essential for vascular development and function. Mural cell loss or malfunction has been associated with numerous diseases including diabetic retinopathy, stroke and amyotrophic lateral sclerosis. In this work, we investigate the role of CDC42 in mural cells <em>in vivo</em>, using the developing mouse retina as a model.</div></div><div><h3>Methods</h3><div>In this study, we generated a mouse model for <em>Cdc42</em> deletion in mural cells by crossing <em>Pdgfrb-CreER</em>^<em>T2</em> mice with <em>Cdc42flox/flox</em> mice. This model (<em>Cdc42</em>^{<em>iΔMC</em>}) allowed us to investigate the role of CDC42 in pericytes and smooth muscle cells in the developing and adult retinal vasculature.</div></div><div><h3>Results</h3><div>We find that, during postnatal development, CDC42 is required in both, pericytes and smooth muscle cells to maintain proper cell morphology, mural cell coverage and distribution. During retinal angiogenesis, <em>Cdc42</em>-depleted pericytes lag behind the sprouting front and exhibit decreased proliferation. Consequently, capillaries at the sprouting front remain pericyte deprived, become dilated and are prone to increased vascular leakage. In addition, arteries and arterioles deviate from their normal growth directions and trajectory. While in the adult retina, mural cell coverage normalizes and pericytes adopt a normal morphology, smooth muscle cell morphologies remain abnormal and arteriolar branching angles are markedly reduced.</div></div><div><h3>Conclusions</h3><div>Our findings demonstrate that CDC42 is required for mural cell migration and proliferation and suggest that mural cells are essential for normal morphogenesis and patterning of the developing retinal vasculature.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107472"},"PeriodicalIF":3.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143459673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vasorelaxant effects of 3-methoxycatechol are not via direct activation of voltage-gated potassium channels","authors":"Rían W. Manville ,&nbsp;Samuel N. Baldwin ,&nbsp;Olivia H. Schaub ,&nbsp;Thomas A. Jepps ,&nbsp;Geoffrey W. Abbott","doi":"10.1016/j.vph.2025.107471","DOIUrl":"10.1016/j.vph.2025.107471","url":null,"abstract":"","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107471"},"PeriodicalIF":3.5,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143400355","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}

{"title":"Effects of FGF-related gene polymorphisms on cerebral infarction in patients treated with direct oral anticoagulants","authors":"Jung Sun Kim ,&nbsp;Minju Park ,&nbsp;Yoon-A Park ,&nbsp;Da Hoon Lee ,&nbsp;Seo-A Choi ,&nbsp;Eun Jeong Jang ,&nbsp;Jeong Yee ,&nbsp;Dong-Hyeok Kim ,&nbsp;Tae-Jin Song ,&nbsp;Junbeom Park ,&nbsp;Hye Sun Gwak","doi":"10.1016/j.vph.2025.107466","DOIUrl":"10.1016/j.vph.2025.107466","url":null,"abstract":"<div><h3>Background</h3><div>The development of cerebral infarction is multifactorial, including both environmental and genetic factors. This study assessed the association between fibroblast growth factor (FGF)-related gene polymorphisms and the incidence of cerebral infarction among patients on direct oral anticoagulants (DOACs).</div></div><div><h3>Methods</h3><div>Patients over 18 years old with atrial fibrillation who were receiving DOACs for cerebral infarction prevention at Ewha Womans University Mokdong Hospital and Ewha Womans University Seoul Hospital were enrolled in this analysis. Twenty-one single nucleotide polymorphisms (SNPs) from <em>FGF1</em>, <em>FGF2</em>, and <em>FGFR1</em> were examined. In multivariable logistic regression analysis, three models (Model I: demographic factors only, Model II: demographic factors and genetic factors, and Model III: genetic factors and the CHA₂DS₂-VASc score) were constructed to identify the risk factors related to cerebral infarction.</div></div><div><h3>Results</h3><div>Among the 536 candidate patients, 21 (3.9 %) experienced cerebral infarction while taking DOACs. From Model I and Model II, age ≥ 75 years and previous thromboembolic event history increased the risk of cerebral infarction. For genetic factors in Model II and III, <em>FGF1</em> rs1596776 GG, <em>FGFR1</em> rs6996321 AA, and FGFR1 rs7012413 TT genotypes were associated with a higher risk of cerebral infarction. The area under the receiver operating curve increased from 0.747 (Model I) to 0.822 (Model II) by adding genetic factors, demonstrating better model performance.</div></div><div><h3>Conclusions</h3><div>This study uncovered the association between <em>FGF</em>-related gene polymorphisms and cerebral infarction among patients with atrial fibrillation undergoing DOAC therapy.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107466"},"PeriodicalIF":3.5,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143383397","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}

{"title":"Protective role of the longevity-associated BPIFB4 gene on cardiac microvascular cells and cardiac aging","authors":"Matteo Calligaris ,&nbsp;Aneta Aleksova ,&nbsp;Alessandra Lucia Fluca ,&nbsp;Milijana Janjusevic ,&nbsp;Giada Carpi ,&nbsp;Daniele Stefanizzi ,&nbsp;Sara Carnevali ,&nbsp;Francesco Curcio ,&nbsp;Annibale Alessandro Puca ,&nbsp;Monica Cattaneo ,&nbsp;Antonio Paolo Beltrami","doi":"10.1016/j.vph.2025.107470","DOIUrl":"10.1016/j.vph.2025.107470","url":null,"abstract":"<div><div>In recent years, the role of the cardiac microvasculature in modulating the symptoms and disease progression of patients affected by cardiac pathology has been reconsidered. The term cardiac microvascular disease (CMD) describes the set of functional and/or structural alterations of the cardiac microvasculature that reduce the ability of the heart to adequately increase its coronary blood flow to keep up with increased metabolic demand. CMD is involved in the evolution of heart disease of both ischemic and non-ischemic origin as well as in cardiac aging. The primary actors involved in this process are the cells of the stromal compartment, whose nature and biology are now investigated to a new level of detail thanks to single-cell omics studies. Recent studies on the genetics of extreme longevity have identified a polymorphic haplotype variant of the BPIFB4 gene that confers prolonged life span and health span, atheroprotective advantages, and an improved immune response.</div><div>The aim of this review was to focus on the beneficial effects of the longevity-associated variant (LAV) of BPIFB4 on cardiac microvascular cell biology, providing novel and exciting mechanisms of its action directed against the development or progression of many age-related cardiovascular diseases, thus emphasizing its translational therapeutic potential.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"158 ","pages":"Article 107470"},"PeriodicalIF":3.5,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143256683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}