Vascular pharmacology最新文献

{"title":"Macrophage and cardiomyocyte roles in cardioprotection: Exploiting the NLRP3 Inflammasome inhibitor INF150","authors":"Magalì Giordano ,&nbsp;Saveria Femminò ,&nbsp;Federica Blua ,&nbsp;Francesca Boccato ,&nbsp;Chiara Rubeo ,&nbsp;Beatrice Mantuano ,&nbsp;Francesca Cioffi ,&nbsp;Stefano Comità ,&nbsp;Arianna Brovero ,&nbsp;Rosa Ciullo ,&nbsp;Massimo Bertinaria ,&nbsp;Claudia Penna ,&nbsp;Pasquale Pagliaro","doi":"10.1016/j.vph.2025.107487","DOIUrl":"10.1016/j.vph.2025.107487","url":null,"abstract":"<div><h3>Background</h3><div>Cardiovascular diseases remain the leading cause of disability and death in the Western world. Effective cardioprotection involves limiting ischemia/reperfusion injury (IRI), including cell death (pyroptosis) driven by the NLRP3 inflammasome. While various cardiac resident cellular populations contribute to cardioprotection, it remains unclear whether targeting resident macrophages is inherently cardioprotective. Given that INF150, an NLRP3 inhibitor, exhibits varying abilities to penetrate cardiomyocytes and macrophages, we sought to address this question.</div></div><div><h3>Methods</h3><div>We studied the cardioprotective potential of INF150, the potent metabolite of the NLRP3 inhibitor INF195, in isolated hearts or cells. In isolated hearts, we measured infarct size, caspase-1 cleavage, and interleukins (IL) release, while in macrophages, naïve H9c2 and differentiated H9c2 cells, we analyzed cell viability, and pyroptosis markers, including IL-1β release and Gasdermin D cleavage, following hypoxia/reoxygenation (H/R).</div></div><div><h3>Results and conclusion</h3><div>While INF150 effectively shielded macrophages from LPS/ATP challenges, it failed to penetrate H9c2 and differentiated H9c2, even at high concentrations (no changes in pyroptosis markers induced by H/R). In the isolated mice heart model, INF150 did not demonstrate cardioprotective effects: infarct size, IL-1β, cleaved caspase-1 levels did not change significantly across tested concentrations of INF150. These findings suggest that while INF150 shows promise in macrophage/phagocytic models, its inability to penetrate cardiomyocytes limits its effectiveness in the whole cardiac tissue. Our results underscore the importance of cardiomyocyte uptake for effective cardioprotection, highlighting the need for NLRP3 inhibitors capable of targeting these cells directly. Future research should focus on enhancing the delivery and cardiomyocyte uptake of NLRP3 inhibitors to achieve cardioprotection. Unlike its precursor, INF195, which penetrates H9c2 cells, INF150 does not appear to offer cardioprotection in the whole organ.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107487"},"PeriodicalIF":3.5,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143651055","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":"PCSK6 ablation in blood circulating cells increases atherosclerotic burden, but improves plaque stability by activating Th17-smooth muscle cell modulatory axis","authors":"Bianca E. Suur ,&nbsp;Glykeria Karadimou ,&nbsp;Colin J.J.M. Willems ,&nbsp;Otto Bergman ,&nbsp;Mariette Lengquist ,&nbsp;Malin Kronqvist ,&nbsp;Roland Baumgartner ,&nbsp;Stephen Malin ,&nbsp;Anton Gisterå ,&nbsp;Göran K. Hansson ,&nbsp;Anders Mälarstig ,&nbsp;Ulf Hedin ,&nbsp;Daniel F.J. Ketelhuth ,&nbsp;Ljubica Matic","doi":"10.1016/j.vph.2025.107490","DOIUrl":"10.1016/j.vph.2025.107490","url":null,"abstract":"<div><h3>Background</h3><div>Proprotein convertase subtilisins/kexins (PCSKs) have been implicated in cancers and cardiovascular disease. We have shown that PCSK6 is a key protease regulating smooth muscle cell (SMC)-mediated vascular remodeling, but also that it can be expressed by T cells and macrophages in atherosclerotic plaques. Whether PCSK6 regulates innate and adaptive immune responses in the context of vascular inflammation is still unknown.</div></div><div><h3>Methods</h3><div>In this study, detailed immunophenotyping of constitutive <em>Pcsk6</em>^{<em>−/−</em>} mice was performed. Bone marrow transplantation into high-cholesterol diet fed <em>Ldlr</em>^{<em>−/−</em>} mice was used to investigate PCSK6-mediated immune effects in atherogenesis and plaque stability.</div></div><div><h3>Results</h3><div>Compared to controls, <em>Pcsk6</em>^{<em>−/−</em>} mice showed higher plasma levels of the chemoattractants CCL2 and CCCL3, and Th17 cytokines IL-17 A and IL-17F<em>. Pcsk6</em> ablation led to increased naïve and effector-memory CD4+ and CD8+ cell numbers in the spleen, and increased release of IL-17 A, IFN-γ and IL-10 as well as proliferation by spleenocytes <em>in vitro</em>. Lack of Pcsk6 also affected innate immunity as macrophages from <em>Pcsk6</em>^{<em>−/−</em>} mice secreted more cytokines, including TNF-α, CCL2, IL-6 and IL-10 upon LPS stimulation <em>in vitro</em>, and were more prone to oxLDL uptake. In line with a pro-inflammatory phenotype, <em>Pcsk6</em>^{<em>−/−</em>}➔<em>Ldlr</em>^{<em>−/−</em>} transplanted mice presented a higher atherosclerotic plaque burden compared to <em>Ldlr</em>^{<em>−/−</em>} receiving control bone marrow. Although larger, <em>Pcsk6</em>^{<em>−/−</em>}➔<em>Ldlr</em>^{<em>−/−</em>} plaques showed increased stability features, including collagen deposition and SMC presence coinciding with significantly increased local levels of the fibrogenic cytokine IL-17.</div></div><div><h3>Conclusions</h3><div>Global <em>Pcsk6</em> ablation leads to the activation of both adaptive and innate immune systems. Interestingly, <em>Pcsk6</em>^{<em>−/−</em>} ablation in bone marrow of hyperlipidemic mice revealed its dual role in atherogenesis, activating a Th17-SMC modulatory axis that promotes plaque stability, despite increased atherosclerotic burden.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107490"},"PeriodicalIF":3.5,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143642801","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":"Measuring contractile forces in vascular smooth muscle cells","authors":"Maia Lyall ,&nbsp;Anna Kamdar ,&nbsp;Robert Sykes ,&nbsp;Badri L. Aekbote ,&nbsp;Nikolaj Gadegaard ,&nbsp;Colin Berry","doi":"10.1016/j.vph.2025.107488","DOIUrl":"10.1016/j.vph.2025.107488","url":null,"abstract":"<div><div>Vascular smooth muscle cell (VSMC) contractility mediates blood vessel tone. Abnormalities in VSMC function and in blood vessel tone can contribute to a variety of cardiovascular diseases. This review examines the role of VSMC contractile force in vascular disease, divided into two primary sections. The first section introducing VSMC mechanical contraction and detailing the molecular mechanisms of VSMC contractility in normal and pathological states. The second section exploring methods of measuring contraction in VSMCs, such as Ca²⁺ imaging, myography, and traction force microscopy, and highlighting where each method is of best use. Understanding the mechanical properties and contractile profiles of VSMCs offers valuable insights into disease mechanisms. By investigating these aspects, this review describes the potential of VSMC contractile forces as diagnostic markers and therapeutic targets in vascular disease.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107488"},"PeriodicalIF":3.5,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143651056","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":"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}