Journal of Vascular Research最新文献

{"title":"N6-methyladenosine (m6A) modification in Vascular Smooth Muscle Disease: A Review.","authors":"Chengjun Huang, Xianping Long, Ranzun Zhao","doi":"10.1159/000548372","DOIUrl":"https://doi.org/10.1159/000548372","url":null,"abstract":"<p><p>: The impairment of vascular smooth muscle cells (VSMCs) causes many vascular diseases, such as atherosclerosis, hypertension, and heart conditions. Research has shown that N6-methyladenosine (m6A) modification regulates s VSMCs ' function in a vascular environment. By regulating RNA metabolism, m6A modification affects key biological processes in VSMCs, such as proliferation, migration, phenotypic transformation, and apoptosis. We aim to examine the role of m6A modification and its associated enzymes in vascular diseases caused by VSMC dysfunction, and explore its potential as a therapeutic target, so that we can develop drugs targeting VSMC dysfunction on a scientific basis.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-14"},"PeriodicalIF":2.3,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evidence in Favour of Calcium-Sensing Receptor(CaSR) in L-cysteine-mediated Vasorelaxation of Mouse Thoracic Aorta.","authors":"Nuran Ogulener, Busra Akarsakarya, Fatma Aydinoglu","doi":"10.1159/000548774","DOIUrl":"https://doi.org/10.1159/000548774","url":null,"abstract":"<p><strong>Introduction: </strong>In our study, the possible role of the calcium-sensing receptor (CaSR) pathway in L-cysteine/Hydrogen sulfide (H2S)-induced vasorelaxations was investigated in isolated mouse thoracic aorta tissue.</p><p><strong>Methods: </strong>For this purpose, vasorelaxations to L-cysteine (H2S substrate; 1 µM -10 mM) and calindol (CaSR agonist; 0.3-10 M) were measured in endothelial-intact and denuded-thoracic aorta segments contracted with phenylephrine (5 M). Also, the effects of propargylglycine (PAG) and calhex-231, cystathionine-gamma-lyase (CSE) and CaSR inhibitor, respectively, on L-cysteine- and calindol-induced vasorelaxations were investigated in thoracic aorta segments. In addition, the effects of L-cysteine, calindol and endothelium on H2S generation in mouse aorta segments were investigated.</p><p><strong>Results: </strong>L-cysteine- and calindol-induced vasorelaxations were reduced in the presence of PAG and calhex231. Furthermore, in endothelium-denuded tissues, the vasorelaxations to calindol and L-cysteine were reduced compared to endothelium-intact tissues. Also, calindol increased basal H2S generation, and PAG and Calhex-231 reduced the increase in H2S production stimulated with calindol. Calhex-231 reduced the increase in H2S production in the presence of L-cysteine. Also, H2S production decreased in endothelium-denuded tissues.</p><p><strong>Conclusion: </strong>In conclusion, endogenous hydrogen sulfide generated by CSE produces endothelium-dependent relaxation by activating CaSR in mouse thoracic aorta tissue.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-19"},"PeriodicalIF":2.3,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunosuppression Drugs Exhibit Differential Effects on Endothelial Cell Function.","authors":"Aly Elezaby, Ryan Dexheimer, David Wu, Sze Yu Chan, Ines Ross Tacco, Ian Y Chen, Nazish Sayed, Karim Sallam","doi":"10.1159/000548353","DOIUrl":"10.1159/000548353","url":null,"abstract":"<p><p>Immunosuppressive medications are widely used to treat patients with neoplasms, autoimmune conditions, and solid organ transplants. Prior studies indicate that immunosuppression drugs can cause adverse vascular remodeling. Given the systemic effects of the drugs, elucidating cell-type specific drug effects has been challenging. We utilized induced pluripotent stem-cell derived endothelial cells to investigate the role of widely used immunosuppression drugs on endothelial function. We found that among immunosuppression agents, sirolimus reduced basic endothelial cell functions including cell migration, proliferation, acetylated LDL uptake, mitochondrial respiration, and angiogenesis properties; while tacrolimus only reduced nitric oxide release. This model allows for investigation of differential effect of immunosuppression drugs on endothelial function that can elucidate mechanisms contributing to adverse vascular profiles observed clinically.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-22"},"PeriodicalIF":2.3,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the Role of Growth Differentiation Factor-15 as a Biomarker of Inflammation in Patients with Atherosclerotic Vascular Disease.","authors":"Joong Min Park, Ian Beckman, Kaye Beckman, Richard B Allan, Christopher L Delaney","doi":"10.1159/000548113","DOIUrl":"10.1159/000548113","url":null,"abstract":"<p><strong>Introduction: </strong>Inflammatory pathways in vascular disease are the focus of intense interest. Multiple studies have shown that interleukin-6 (IL-6) is strongly implicated in the atherosclerotic process. Accumulating evidence suggests a similar role for growth differentiation factor-15 (GDF-15).</p><p><strong>Methods: </strong>In this study, we measured and compared circulating levels of IL-6 and GDF-15 in a cohort of 20 vascular surgical patients with atherosclerotic disease presenting for surgical revascularization (carotid endarterectomy or common femoral artery endarterectomy) and in a similar number of age-matched healthy volunteers. A cross-sectional analysis of prospectively collected data was performed, with serum GDF-15 and IL-6 levels measured and assessed using enzyme-linked immunosorbent assays (ELISAs).</p><p><strong>Results: </strong>We observed substantial circulating levels of GDF-15 in most patients (17/20) compared to the reference range upper limit of 1,500 pg/mL, irrespective of the type of vascular disease and revascularization procedure they were undergoing. In contrast, only 1 healthy control participant had a borderline high GDF-15 of 1,572 pg/mL. Indeed, the mean serum GDF-15 level between patients (2,515 pg/mL, SD 906) and healthy controls (1,016 pg/mL, SD 219) was highly significant (p value <0.001). On the other hand, although IL-6 levels between patients (mean 3.6, SD 2.54 pg/mL) and healthy controls (mean 2.2, SD 0.67 pg/mL) were significantly different (p = 0.020), only 7 patients had values above the reference range upper limit of 3.4 pg/mL.</p><p><strong>Conclusion: </strong>These results suggest that serum GDF-15, but not IL-6, is a strong candidate for use as a biomarker of atherosclerotic vascular disease and may allow for earlier risk factor modification to help prevent disease onset and progression. Large-scale studies aimed at determining whether a rising GDF-15 is an indication of worsening outcome in a wider spectrum of patients with vascular disease are clearly warranted.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-11"},"PeriodicalIF":2.3,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deficiency of p27^kip1, a Cyclin-Dependent Kinase Inhibitor, Accelerates Topical Elastase/3-Aminopropionitrile Fumarate Salt-Induced Abdominal Aortic Aneurysm Development in Mice.","authors":"Keisuke Kamada, Hong Niu, Shinsuke Kikuchi, Nobuyoshi Azuma, Gale L Tang","doi":"10.1159/000547829","DOIUrl":"10.1159/000547829","url":null,"abstract":"<p><p><p>Introduction: Abdominal aortic aneurysm (AAA) is a multifactorial disease with limited identification of contributing genetic factors. p27kip, also known as CDKN1B, is a cell cycle inhibitor that regulates vascular smooth muscle cells (VSMCs) and macrophages (Mϕ). The role of p27 in AAA development was assessed by AAA induction in p27 knockout (p27-/-) and wild-type (WT) mice.</p><p><strong>Methods: </strong>AAAs were induced in male and female p27-/- and WT mice via topical elastase with oral administration of 3-aminopropionitrile fumarate salt. Aortic diameter was measured with ultrasound. VSMCs and macrophages were quantified by immunohistochemistry. Oxidative stress genes were analyzed using polymerase chain reaction. In vitro cell proliferation, migration, and oxidative stress assay were performed on VSMCs isolated from abdominal aortas.</p><p><strong>Results: </strong>p27-/- mice developed significantly larger AAA diameter than WT mice with reduced VSMCs and increased macrophages. M1ϕ were significantly elevated in p27-/- mice, while M2ϕ were more abundant in WT mice. p27-/- mice had lower expression of the antioxidant gene, Nrf2. In vitro experiments demonstrated increased proliferation and migration in p27-/- cells with increased oxidative stress sensitivity.</p><p><strong>Conclusion: </strong>Knockout of p27 accelerated aneurysm growth with increased macrophage infiltration, VSMC loss, and decreased antioxidant factors, highlighting a potential role for p27 in AAA progression. </p>.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-13"},"PeriodicalIF":2.3,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511535/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vasomotion in Human Fingers.","authors":"Pekka Talke, Jonathan S Maltz, Marcus Talke, Mika Scheinin, Mohamed Kheir Diab","doi":"10.1159/000548155","DOIUrl":"10.1159/000548155","url":null,"abstract":"<p><strong>Introduction: </strong>We describe methods by which vasomotion can be recorded in awake and anesthetized human subjects without significant interference from other spontaneous vascular oscillations.</p><p><strong>Methods: </strong>In three separate studies, we used photoplethysmography (PPG) to record vasomotion in fingertips. In Study 1, we induced chemical sympathectomy in the studied hand of 11 awake subjects who received intravenous dexmedetomidine infusions. In Study 2, we administered four progressively increasing intravenous dexmedetomidine infusions to 16 awake volunteers. In Study 3, we recorded vasomotion simultaneously from 6 fingers of 7 patients who were under dexmedetomidine-based anesthesia. Five-minute epochs of PPG recordings that displayed slow vascular oscillations were analyzed for frequency and amplitude.</p><p><strong>Results: </strong>In Study 1, vasomotion frequencies were 0.025 ± 0.008 Hz. In Study 2, vasomotion frequencies were 0.033 ± 0.006 Hz, and 0.032 ± 0.008 Hz during the two highest dexmedetomidine infusion steps. In Study 3, vasomotion frequencies ranged from 0.020 to 0.037 Hz and were observed in all 6 fingers, with no synchrony between the six fingers.</p><p><strong>Conclusion: </strong>The vascular oscillations we observed without significant interference from other spontaneous oscillations are independent of neural activity (Study 1), local in nature (Study 3), and associated with alpha-2-adrenoceptor activation, consistent with known properties of vasomotion.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-15"},"PeriodicalIF":2.3,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144959076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring Potential Causality and Molecular Mechanisms between Heart Failure and Renal Failure: Insights from Mendelian Randomization Studies, the MIMIC-IV Database and the Gene Expression Omnibus Database.","authors":"Shaoyi Peng, Hailong Li, Kaiyuan Li","doi":"10.1159/000548035","DOIUrl":"10.1159/000548035","url":null,"abstract":"<p><strong>Introduction: </strong>Heart failure (HF) and renal failure (RF) frequently coexist as cardiorenal syndrome, but their underlying causal mechanisms remain poorly defined.</p><p><strong>Methods: </strong>This study applied Mendelian randomization (MR) using genome-wide association study (GWAS) datasets to investigate the causal effect of HF on RF. The inverse variance weighted method assessed causality, and summary-data-based MR (SMR) was used to identify therapeutic targets. Additional analyses included 211 gut microbiota traits and 1,400 serum metabolites. Validation was performed using the MIMIC-IV database. Transcriptomic data were analyzed to identify differentially expressed genes (DEGs) and key transcription factors (TFs).</p><p><strong>Results: </strong>This study found that HF significantly increases the risk of RF (OR = 1.54, 95% CI: 1.07-2.23, p = 0.020). SMR analysis identified SURF1 and MAP3K11 as potential therapeutic targets for HF and RF. One gut microbiota genus and one serum metabolite showed causal associations with both diseases. MIMIC-IV data supported the HF-RF association (OR = 2.94, 95% CI: 2.81-3.07, p < 0.001). A total of 11 overlapping DEGs were enriched in the MAPK cascade, with RELA identified as a key TF.</p><p><strong>Conclusion: </strong>This study provides genetic and molecular evidence supporting a causal role of HF in RF, highlighting microbial, metabolic, and immune mechanisms as potential therapeutic targets.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-21"},"PeriodicalIF":2.3,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144959006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A State-Wide Retrospective Cohort Study Examining Effects of Transfusing Old Blood Products in Vascular Surgical Patients.","authors":"Nchafatso Obonyo, Lawrence Lu, Zohaib Nadeem, Zahra Hosseinzadeh, Reema Rachakonda, Nicole White, Declan Sela, Matthew Tunbridge, Beatrice Sim, Louise See Hoe, Yogeesan Sivakumaran, Gianluigi Li Bassi, Jonathon Fanning, John-Paul Tung, Jacky Suen, John Fraser","doi":"10.1159/000548049","DOIUrl":"10.1159/000548049","url":null,"abstract":"<p><strong>Introduction: </strong>We investigated the effects of transfusing blood products close to the expiration date (i.e., ≥35 days packed red blood cells [PRBCs] and >3 days platelets [PLTs]) on vascular patients.</p><p><strong>Methods: </strong>We retrospectively examined all PRBC and PLT transfusions in patients who underwent vascular procedures without cardiopulmonary bypass in Queensland from 2007 to 2013. Mortality, length of stay (LOS), and blood product quantities were compared in patients transfused exclusively with PRBCs <21 days vs. PRBCs ≥35 days and PLTs ≤3 days vs. PLTs >3 days.</p><p><strong>Results: </strong>No significant mortality difference was found between patients transfused fresh vs. old PRBCs (26/493 [5.3%] vs. 6/152 [3.9%]; OR 0.75; 95% CI: 0.3-1.9). Patients transfused fresh PRBCs experienced a longer LOS (11 days [IQR: 7-20] vs. 10 days [IQR: 7-15]; 95% CI: -4.8 to -0.24) and more PRBC units (3.9 ± 4.5 units vs. 2.1 ± 1.3 units; 95% CI: -2.3 to -0.9). Among patients transfused PLTs, there were no significant differences in mortality (24/124 [19.4%] vs. 14/78 [17.9%]; OR 1.0; 95% CI: 0.5-2.3) between patients transfused fresh vs. old PLTs.</p><p><strong>Conclusion: </strong>Within the limitations of the retrospective study design, transfusion of older PRBCs or PLTs was associated with fewer transfused units, shorter hospital stays, but no difference in mortality.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-8"},"PeriodicalIF":2.3,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503803/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144959259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposure to Artificial Light at Night Alters Ultradian Rhythms in Endothelial Function.","authors":"James C Walton, O Hecmarie Meléndez-Fernández, A Courtney DeVries, Paul D Chantler, Randy J Nelson","doi":"10.1159/000547915","DOIUrl":"10.1159/000547915","url":null,"abstract":"<p><strong>Introduction: </strong>Endogenous biological timing mechanisms are fundamental aspects of living cells, tissues, and organisms. Virtually every aspect of physiology and behavior is mediated by self-sustaining circadian clocks, which depend on light to synchronize with the external daily environment. However, exposure to artificial light at night (ALAN) can impair temporal adaptations and affect health and disease.</p><p><strong>Methods: </strong>During a study of the effects of long-term ALAN exposure on cardiovascular function, we serendipitously detected ultradian rhythms in muscarinic receptor dependent relaxation of isolated aortic tissue.</p><p><strong>Results and conclusion: </strong>Mice exposed to dark nights displayed an ultradian pattern of maximum endothelial-dependent relaxation that was antiphase between the sexes. Rhythmic patterns of relaxation were abolished by ALAN exposure in both sexes suggesting that ALAN exposure can affect ultradian rhythms in physiology and behavior.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-7"},"PeriodicalIF":2.3,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12439349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144816959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Qsox1 Contributes to Vascular Remodelling in Response to Hypertension.","authors":"Malha Sadoune, Jérome Mourad, Céline Luc, Hélène Ragot, Philippe Mateo, Evelyne Polidano, Alain Cohen-Solal, Sylvanna Dorrifourt, Zhenlin Li, Jane-Lise Samuel, Alexandre Mebazaa, Anais Caillard","doi":"10.1159/000546331","DOIUrl":"10.1159/000546331","url":null,"abstract":"<p><strong>Introduction: </strong>QSOX1, a sulfhydryl oxidase involved in arterial remodelling, has recently emerged as a biomarker for preeclampsia and acute heart failure. This study sought the cardiovascular roles of Qsox1 in response to angiotensin II (AngII)-induced hypertension.</p><p><strong>Methods: </strong>With approval from an Animal Ethics Committee (CNREEA#9), two models were developed: Qsox1-invalidated adult male mice (Qsox1-/-) mice (C57BL/6J background) and a tamoxifen-inducible, vascular smooth muscle cell (VSMC)-specific Qsox1 knockout. Hypertension was induced via AngII minipumps and trans-aortic constriction, with assessments of cardiac function, vessel size, and VSMC phenotype.</p><p><strong>Results: </strong>Qsox1-/- at baseline had lower blood pressure and exhibited a synthetic/immature VSMC phenotype in coronary arteries when compared to wild-type (WT). After 4 weeks of AngII infusion, Qsox1-/- mice showed acute heart failure, absent coronary media hypertrophy, and increased perivascular fibrosis compared to hypertensive WT controls (p < 0.01). VSMC-specific Qsox1 knockout leading to the lack of Qsox1 in VSMC only impairs the phenotype of these cells without effecting cardiac function in response to AngII.</p><p><strong>Conclusion: </strong>These data implicate vascular Qsox1 in the adaptive mechanisms of VSMC to pressure overload such as the development of media hypertrophy.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-15"},"PeriodicalIF":2.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}