Vascular pharmacology最新文献

{"title":"Exploring the interplay between valvular and serum zinc and copper levels and disease markers in aortic stenosis","authors":"Bartłomiej Perek ,&nbsp;Piotr Rzymski ,&nbsp;Aleksandra Proch ,&nbsp;Mateusz Puślecki ,&nbsp;Barbara Poniedziałek ,&nbsp;Andrzej Fal ,&nbsp;Anna Komosa ,&nbsp;Marek Jemielity ,&nbsp;Przemysław Niedzielski","doi":"10.1016/j.vph.2025.107497","DOIUrl":"10.1016/j.vph.2025.107497","url":null,"abstract":"<div><div>Aortic stenosis (AS) is a progressive condition characterized by valve calcification and significant morbidity, often requiring invasive intervention. The AS pathophysiology is multifaceted, with evidence suggesting a role for trace elements. However, whether zinc (Zn) and copper (Cu) are associated with valve calcification is unclear. This exploratory study assessed the Zn and Cu levels in the serum and aortic valves of AS patients undergoing surgical valve replacement and explored the relationships between trace elements and clinical and biochemical parameters to better understand their potential roles in AS pathophysiology. An inverse relationship was observed between serum Zn levels and systolic pressure gradients across the valve (<em>p</em> &lt; 0.0001). Zn accumulation was identified in calcified aortic valves, suggesting a systemic redistribution of Zn during disease progression. The valvular Cu/Zn ratio was reversed (&lt;1) compared to that in serum. The lipoprotein(a), an inflammatory marker, was positively correlated with serum Cu levels (<em>p</em> = 0.0007) and the Cu/Zn ratio (<em>p</em> = 0.02). However, no direct association was found between valvular Cu content and the AS severity. The findings suggest that Zn depletion in serum, coupled with its accumulation in calcified valves, reflects a disease-driven redistribution mechanism that may serve a protective role against calcification progression. Additionally, the study highlights a potential interplay between Cu metabolism and inflammatory processes in AS. Further research is required to determine whether therapeutic modulation of Zn levels could offer benefits in AS management.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107497"},"PeriodicalIF":3.5,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870747","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":"Ceramide-based risk score: A novel laboratory tool for cardiovascular risk stratification in hyperuricemia and gout","authors":"Aleš Kvasnička ,&nbsp;David Friedecký ,&nbsp;Barbora Piskláková ,&nbsp;Jakub Rozhon ,&nbsp;Karel Pavelka ,&nbsp;Blanka Stibůrková","doi":"10.1016/j.vph.2025.107495","DOIUrl":"10.1016/j.vph.2025.107495","url":null,"abstract":"<div><div>Gout and hyperuricemia increase cardiovascular disease risk, highlighting the need for improved risk stratification. In this pilot study, we evaluated the Coronary Event Risk Test (CERT) in 94 hyperuricemic and 196 gout patients, and 53 controls. Plasma ceramides were determined by liquid chromatography–mass spectrometry. Elevated CERT scores (≥7) occurred in 11.7 % (2-fold increase) of hyperuricemic and 31.12 % (5.5-fold increase) of gout patients compared to controls. Additionally, both hyperuricemic and gout patients with increased CERT also exhibited higher levels of inflammation and atherogenic index of plasma, both of which were significantly associated with CERT. Incorporating CERT into routine care may enhance risk stratification and guide targeted interventions in this patient population.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107495"},"PeriodicalIF":3.5,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143835082","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":"Epitranscriptomics in atherosclerosis: Unraveling RNA modifications, editing and splicing and their implications in vascular disease","authors":"Victoria Stopa ,&nbsp;Dimitra Dafou ,&nbsp;Korina Karagianni ,&nbsp;A. Yaël Nossent ,&nbsp;Rosienne Farrugia ,&nbsp;Yvan Devaux ,&nbsp;Miron Sopic ,&nbsp;AtheroNET COST Action CA21153 (www.atheronet.eu)","doi":"10.1016/j.vph.2025.107496","DOIUrl":"10.1016/j.vph.2025.107496","url":null,"abstract":"<div><div>Atherosclerosis remains a leading cause of morbidity and mortality worldwide, driven by complex molecular mechanisms involving gene regulation and post-transcriptional processes. Emerging evidence highlights the critical role of epitranscriptomics, the study of chemical modifications occurring on RNA molecules, in atherosclerosis development. Epitranscriptomics provides a new layer of regulation in vascular health, influencing cellular functions in endothelial cells, smooth muscle cells, and macrophages, thereby shedding light on the pathogenesis of atherosclerosis and presenting new opportunities for novel therapeutic targets. This review provides a comprehensive overview of the epitranscriptomic landscape, focusing on key RNA modifications such as N6-methyladenosine (m6A)<strong>,</strong> 5-methylcytosine (m⁵C)<strong>,</strong> pseudouridine (Ψ), RNA editing mechanisms including A-to-I and C-to-U editing and RNA isoforms. The functional implications of these modifications in RNA stability, alternative splicing, and microRNA biology are discussed, with a focus on their roles in inflammatory signaling, lipid metabolism, and vascular cell adaptation within atherosclerotic plaques. We also highlight how these modifications influence the generation of RNA isoforms, potentially altering cellular phenotypes and contributing to disease progression. Despite the promise of epitranscriptomics, significant challenges remain, including the technical limitations in detecting RNA modifications in complex tissues and the need for deeper mechanistic insights into their causal roles in atherosclerotic pathogenesis. Integrating epitranscriptomics with other omics approaches, such as genomics, proteomics, and metabolomics, holds the potential to provide a more holistic understanding of the disease.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107496"},"PeriodicalIF":3.5,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143835083","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":"Efficacy of beta-blocker agents on clinical outcomes in patients with thoracic aortic aneurysm: A systematic review and meta-analysis of randomized controlled trials","authors":"Lokman H. Tanriverdi ,&nbsp;Annie Barrett ,&nbsp;Asanish Kalyanasundaram ,&nbsp;Mohammad A. Zafar ,&nbsp;Bulat A. Ziganshin ,&nbsp;John A. Elefteriades","doi":"10.1016/j.vph.2025.107494","DOIUrl":"10.1016/j.vph.2025.107494","url":null,"abstract":"<div><h3>Objective</h3><div>Studies investigating the efficacy of β-blocker agents for patients with thoracic aortic aneurysm (TAA) have produced heterogeneous and conflicting results. We assess the effects of β-blockers on clinical outcomes in patients with TAA.</div></div><div><h3>Methods</h3><div>A systematic literature search was performed through Ovid MEDLINE, EMBASE, Web of Science, Pubmed and Cochrane CENTRAL, all from inception to April 30, 2024. Randomized controlled trials (RCTs) exploring the effect of β-blocker agents in patients with TAA were considered for inclusion, with no population restriction. Inverse variance–weighted random-effects model was used. The overall risk of bias assessment was conducted by Cochrane Risk of Bias 2 tool. The primary outcome was aortic events during follow-up.</div></div><div><h3>Results</h3><div>We included a total of 161 patients with TAA (mean age, 27.6 years; 80 [49.7 %] male, mean follow-up 6.7 years) in 4 RCTs. The pooled risk ratio in the β-blocker arm for aortic events was 0.74 [95 % CI (0.20; 2.71), I²: 0 %, <em>p</em> = 0.64, low certainty of evidence (CoE)] when compared to placebo or no treatment in patients with TAA. The pooled risk ratios for aortic dissection or death (all-cause mortality) or in the β-blocker arm were 0.45 (95 % CI (0.10; 1.98), I²: 0 %, <em>p</em> = 0.29, low CoE) and 0.58 (95 % CI (0.15; 2.24), I²: 0 %, <em>p</em> = 0.43, low CoE), respectively. The risks of aortic dissection, rupture, or death were comparable, regardless of agent, disease, and age.</div></div><div><h3>Conclusion</h3><div>We found no evidence of benefit from β-blocker treatment for patients with TAA. More robust RCTs are needed to establish evidence-based recommendations.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107494"},"PeriodicalIF":3.5,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143807712","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":"IL-1β inhibition in stabilizing atherosclerotic plaques: The critical role of fibroblast-like cells","authors":"He Xu ,&nbsp;Judith Sluimer","doi":"10.1016/j.vph.2025.107493","DOIUrl":"10.1016/j.vph.2025.107493","url":null,"abstract":"<div><div>Targeting interleukin-1 beta (IL-1β) to mitigate inflammation is known to stabilize atherosclerotic plaques, thereby lowering the risk of acute cardiovascular events. The precise mechanisms are not yet known.</div><div>Fideler et al. examined the effects of IL-1β on exaggerated atherosclerosis following clonal hematopoiesis of indeterminate potential (CHIP). Unexpectedly, they showed an effect of IL-1β blockage on fibroblast-like cells and their role in the progression of atherosclerosis in the presence of CHIP. Here, we discuss these findings and place them in context of current insights on plaque fibroblast identity and function. While single cell sequencing studies had observed the presence of plaque fibroblasts in atherosclerotic plaques, their function has yet to be unraveled. By focusing on both in vitro and ex vivo models, the research explored how IL-1β stimulation drives functional and molecular changes in fibroblast-like cells, such as increased cytokine production and enhanced matrix degradation, which replicate the inflammatory microenvironment commonly seen in atherosclerotic lesions. Furthermore, the study suggests that inhibiting IL-1β might encourage the accumulation of fibroblast-like cells within the fibrous cap, a process that could improve plaque stability by reducing inflammatory activity and strengthening the structural integrity of the plaque. Depletion of proteoglycan 4 (Prg4) -positive cells, that represent fibroblasts amongst other cell types, reduced cap thickness in atherosclerosis with clonal hematopoiesis of indeterminate potential.</div><div>The findings suggest that IL-1β not only plays a critical role in promoting inflammation, but also in altering the phenotype of fibroblast-like cells, contributing to the destabilization of atherosclerotic plaques. This study is the first to show a function of plaque fibroblast-like cells in exaggerated atherosclerosis following clonal hematopoiesis of indeterminate potential. Future studies should confirm this effect in models without clonal hematopoiesis of indeterminate potential, and with fibroblast depletion based on more specific fibroblast genes.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107493"},"PeriodicalIF":3.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143776437","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":"TRPV4 in Cerebral Small Vessel Disease: A key interacting partner","authors":"Sara M.P. Lambrichts ,&nbsp;Robert J. van Oostenbrugge ,&nbsp;Sébastien Foulquier","doi":"10.1016/j.vph.2025.107492","DOIUrl":"10.1016/j.vph.2025.107492","url":null,"abstract":"<div><div>Cerebral small vessel disease (cSVD) is a major cause of vascular cognitive impairment and dementia. The underlying disease mechanisms are centered around the dysfunction of the neurovascular unit and include an impairment of the blood-brain barrier (BBB) permeability, a decreased cerebrovascular reactivity and cerebral hypoperfusion. The cells composing the neurovascular unit express a wide variety of mechanosensitive ion channels that are relevant for these processes. Recent research has increasingly focused on the mechanobiology of cerebral microvessels with recent evidence pointing towards a significant role of transient receptor potential vanilloid 4 (TRPV4). This Ca²⁺-permeable channel regulates key physiological functions, including vascular tone, angiogenesis, BBB integrity and neuroinflammation. Beyond its physiological role, recent evidence implicates TRPV4 in pathological processes such as cerebrovascular remodelling, impaired cerebrovascular reactivity, and BBB dysfunction. In this review, we explore the multiple roles of TRPV4 within the neurovascular unit, its interactions with key molecular partners, and we discuss evidence for its potential contribution to cSVD.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107492"},"PeriodicalIF":3.5,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143671179","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":"Clinical translation of mesenchymal stem cells in ischemic heart failure: Challenges and future perspectives","authors":"Anqi Guan ,&nbsp;Lisa Alibrandi ,&nbsp;Elika Verma ,&nbsp;Niketa Sareen ,&nbsp;Qingdong Guan ,&nbsp;Vincenzo Lionetti ,&nbsp;Sanjiv Dhingra","doi":"10.1016/j.vph.2025.107491","DOIUrl":"10.1016/j.vph.2025.107491","url":null,"abstract":"<div><div>Myocardial infarction (MI) with resulting congestive heart failure is one of the leading causes of death worldwide. Current therapies for treating MI, such as devices, traditional medicine, and surgeries, come with many limitations as patients in their final stages of heart failure have little chances of experiencing any reversible changes. In recent decades, Mesenchymal stem cell (MSC) based therapy has become one of the most popular and rapidly developing fields in treating MI. Their supremacy for clinical applications is partially due to their unique properties and encouraging pre-clinical outcomes in various animal disease models. However, the majority of clinical trials registered for MSC therapy for diverse human diseases, including MI, have fallen short of expectations. This review intends to discuss the recent advances in the clinical application of using MSCs for cardiac repair and discuss challenges facing the clinical translation of MSCs for cardiac regeneration such as restoration of endothelial-cardiomyocyte crosstalk, immunomodulation and immune rejection, poor homing and migration, as well as low retention and survival. Furthermore, we will discuss recent strategies being investigated to help overcome some of these challenges.</div></div>","PeriodicalId":23949,"journal":{"name":"Vascular pharmacology","volume":"159 ","pages":"Article 107491"},"PeriodicalIF":3.5,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143671178","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":"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}