Journal of Vascular Research最新文献

{"title":"Effects of Exercise Mode and Intensity on Retinal Microvascular Structure and Function in Heart Failure Patients with Preserved Ejection Fraction: A Pilot Exercise Intervention Trial.","authors":"Lukas Streese, Egbert Thomas Ritter, Raphael Schoch, Julia Maria Kröpfl, Christoph Hauser, Benedikt Gasser, Thomas Dieterle, Arno Schmidt-Trucksäss, Henner Hanssen","doi":"10.1159/000553072","DOIUrl":"10.1159/000553072","url":null,"abstract":"<p><strong>Introduction: </strong>We aimed to investigate the effect of different exercise modes on retinal microvascular endothelial function in patients with HF with preserved ejection fraction (HFpEF).</p><p><strong>Methods: </strong>Twenty-eight patients were randomly allocated to either a moderate (MCT) or high-intensity interval training (HIIT) group for 12 weeks. Retinal microvascular structure and function were investigated by analyzing central retinal arteriolar (CRAE) and venular (CRVE) diameter equivalents, the arteriolar-to-venular diameter ratio (AVR), and the dynamic arteriolar (aFID) and venular (vFID) flicker light-induced dilation response.</p><p><strong>Results: </strong>Twenty patients (mean age 70 ± 9 years) were included in the final analysis. After HIIT, AVR increased (0.80 ± 0.03 vs. 0.83 ± 0.04, p = 0.03) due to arteriolar widening. CRAE increased (157 ± 18 µm vs. 164 ± 18 µm, p = 0.05), but CRVE did not change (196 ± 27 µm vs. 197 ± 24 µm, p = 0.56). After MCT, AVR also increased (0.80 ± 0.08 vs. 0.83 ± 0.06, p = 0.02) without significant changes in CRAE (160 ± 19 µm vs. 165 ± 18 µm, p = 0.07) or CRVE (201 ± 14 µm vs. 199 ± 14 µm, p = 0.40). aFID improved after MCT (2.1 ± 1.6% vs. 3.1 ± 1.8%, p = 0.03) but not after the HIIT intervention (2.1 ± 1.7% vs. 2.4 ± 2.1%, p = 0.60). vFID did not statistically significant change neither in the HIIT (4.4 ± 2.2% vs. 3.4 ± 1.9%, p = 0.06) nor in the MCT (4.3 ± 2.2% vs. 5.5 ± 4.1%, p = 0.26) group.</p><p><strong>Conclusion: </strong>MCT and HIIT are both adequate therapy options to improve microvascular health in patients with HFpEF.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-11"},"PeriodicalIF":1.3,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13432933/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148265093","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":"Hemodynamic Stress as a Cause of the High Prevalence of Arterial Disease in Women.","authors":"Almut Schreiber, Ulrich Barz, Helmut Barz","doi":"10.1159/000552946","DOIUrl":"10.1159/000552946","url":null,"abstract":"<p><strong>Background: </strong>Intracranial aneurysms, spontaneous coronary artery dissection, and fibromuscular dysplasia are significantly more common in women than in men, but the cause of these diseases and the cause of the predominance in women are unknown. It is also unclear whether and how genetic factors (genetic disposition or genetic pleiotropy) can influence the development of these diseases. A literature search in PubMed was conducted to identify the causes of the three arterial diseases. Particular attention was paid to the hemodynamic load on the arteries.</p><p><strong>Summary: </strong>The imbalance of body fluids in pregnancy, menstruation, and premenstrual syndrome contributes to structural changes in the arterial wall and can promote arterial diseases.</p><p><strong>Key messages: </strong>Increase in blood volume, high blood flow velocity, and edema of the vessel wall are factors that contribute to arterial diseases and can explain the predominance of some arterial diseases in women. These hemodynamic factors are to be distinguished from genetic causes, arteriosclerosis, or inflammatory diseases.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-10"},"PeriodicalIF":1.3,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13472596/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148239352","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":"Stage-Associated MicroRNA Expression Patterns in Human Great Saphenous Veins across Chronic Venous Disease Severity.","authors":"Leonardo Oliveira Pimentel, Eduardo Abrão Spinola Rezk, Matheus Bertanha, Ricardo de Alvarenga Yoshida, Jan Janzen, Tainara Francine Felix, Márcio de Carvalho, Rainer M Lopez Lapa, Lenize Silva Rodrigues, Patricia Pintor Reis, Iael Weissberg Minutentag, Winston Bonetti Yoshida","doi":"10.1159/000553000","DOIUrl":"10.1159/000553000","url":null,"abstract":"<p><strong>Introduction: </strong>Chronic venous disease (CVD) is characterized by progressive venous wall remodeling, extracellular matrix dysregulation, and chronic inflammation. MicroRNAs (miRNAs) regulate vascular processes, but their expression in human venous tissue across disease stages remains incompletely defined. We evaluated global miRNA expression in great saphenous veins across CVD severity.</p><p><strong>Methods: </strong>In this cross-sectional pilot study, paraffin-embedded vein samples were obtained from patients with CVD and classified according to CEAP criteria into early-stage (C2-C3; G1) and advanced-stage (C4-C5; G2). Vein segments from patients without venous reflux undergoing arterial revascularization served as controls. Global miRNA expression profiling was performed using the GeneChip® miRNA 4.0 Array with multiple-testing correction. Direct statistical comparison between G1 and G2 was not performed.</p><p><strong>Results: </strong>Twenty-seven samples were analyzed (6 controls, 12 G1, 9 G2). A total of 155 miRNAs were significantly dysregulated in CVD compared with controls. Most miRNAs were detected in both G1 and G2 comparisons, whereas 36 were identified only in the G1 vs. control comparison and two (hsa-miR-7977 and hsa-miR-23a-5p) only in the G2 vs. control comparison.</p><p><strong>Conclusion: </strong>miRNA profiling suggests stage-associated expression patterns in human saphenous veins, indicating early molecular remodeling during CVD progression. These findings are exploratory and require independent validation.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-10"},"PeriodicalIF":1.3,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148239400","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":"Vascular Ageing in Conditions Associated with Early-Onset Hypogonadism.","authors":"Angela K Lucas-Herald, Jane D McNeilly, S Faisal Ahmed","doi":"10.1159/000552685","DOIUrl":"10.1159/000552685","url":null,"abstract":"<p><strong>Introduction: </strong>Early-onset hypogonadism may increase the risk of early vascular ageing (EVA).</p><p><strong>Methods: </strong>Boys with conditions linked to intrauterine hypogonadism - Klinefelter syndrome (KS) and hypospadias - were recruited alongside healthy controls. Assessments included clinic blood pressure (BP), flow-mediated dilatation, carotid intima-media thickness (CIMT), and pulse wave velocity. Fasting blood tests measured testosterone, anti-Müllerian hormone, luteinising hormone, follicle-stimulating hormone, triglycerides, glucose, and cholesterol. Oxidative stress and epigenetic markers were evaluated using total antioxidant capacity (TAOC), peroxide, oxidative stress index (OSI), 8-hydroxydeoxyguanosine (8-OHdG), thiobarbituric acid reactive substances (TBARS), glutathione, alpha klotho protein, histone H3 modification, telomerase, and DNA methyltransferase (DNMT) activity.</p><p><strong>Results: </strong>Eleven boys per group were studied (median age: 14.5 years). Systolic BP was higher in KS and hypospadias compared with controls. CIMT and pulse pressure were elevated in hypospadias versus controls. Mean arterial pressure was increased in KS. Oxidative stress markers (TBARS, TAOC, peroxide, and OSI) were higher in hypospadias. 8-OHdG was elevated in hypospadias versus controls but lower than in KS. DNMT activity was increased in both KS and hypospadias. No differences were observed in alpha klotho, histone H3 modification, or telomerase.</p><p><strong>Conclusion: </strong>Adolescents with early-onset hypogonadism show evidence of EVA, with associated oxidative stress and epigenetic alterations warranting further investigation.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-10"},"PeriodicalIF":1.3,"publicationDate":"2026-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148005694","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":"Mediastinal Lymphadenopathy as a Prognostic Marker in Acute Pulmonary Embolism.","authors":"Hans-Jonas Meyer, Mattes Hinnerichs, Anar Aghayev, Daniele Romeo, Yazan Mehsin, Saher Saeed, Jan Borggrefe, Alexey Surov","doi":"10.1159/000552631","DOIUrl":"10.1159/000552631","url":null,"abstract":"<p><strong>Introduction: </strong>Computed tomography (CT) is the modality of choice to diagnose acute pulmonary embolism (PE). The present multicentric study aimed to demonstrate the prognostic role of mediastinal lymphadenopathy for short mortality within 30 days in patients with acute PE.</p><p><strong>Methods: </strong>The investigated patient sample comprised 935 patients (411 female, 44%) with a mean age of 65.3 ± 16.3 years derived from three academic centers. Contrast-enhanced CT pulmonalis angiography was used to assess the presence of mediastinal lymphadenopathy. The primary end point of this study was 30-day mortality. The Simplified Pulmonary Embolism Severity Index (sPESI) was calculated as a clinical prognostic score.</p><p><strong>Results: </strong>A total of 98 patients (10.5%) died within the 30-day observation period. Mediastinal lymphadenopathy was present in a total of 171 cases (18.3%). Mediastinal lymphadenopathy was associated with 30-day mortality with an odds ratio (OR) of 1.83 (95% confidence interval [CI], 1.12-2.92; p = 0.013 in univariable analysis) and 1.67 (95% CI, 1.01-2.69; p = 0.041 in multivariable analysis).</p><p><strong>Conclusion: </strong>Mediastinal lymphadenopathy represents an independent prognostic factor for 30-day mortality in patients with acute PE. The underlying pathophysiological mechanisms remain unclear and should be further investigated.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-6"},"PeriodicalIF":1.3,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147982188","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":"Inhibition of H₂S Production Reduces Portal Pressure and Attenuates Liver Fibrosis in Bile Duct-Ligated Rats.","authors":"Raffaele Buono, Marika Crescenzi, Alessandra Brocca, Arben Dedja, Jessica Gasparello, Matteo Fassan, Massimo Bolognesi, Marco Di Pascoli","doi":"10.1159/000552592","DOIUrl":"10.1159/000552592","url":null,"abstract":"<p><strong>Introduction: </strong>Hydrogen sulfide (H₂S) is a gaseous signalling molecule with vasodilatory properties and regulates inflammation and fibrosis in the liver.</p><p><strong>Methods: </strong>Rats with bile duct ligation (BDL)-induced liver disease were treated with propargylglycine (PAG; 30 mg/kg via intragastric gavage), a selective inhibitor of cystathionine γ-lyase, the main source of H₂S in the cardiovascular system and liver, or vehicle. PAG treatment was initiated at day 5 after BDL to evaluate its effects on the progression of liver fibrosis and portal hypertension.</p><p><strong>Results: </strong>In BDL rats, PAG significantly reduced portal pressure (PP) (10.4 ± 2.7 mm Hg versus 16.0 ± 3.9 mm Hg, p < 0.05) without affecting systemic pressure. In mesenteric arteries mounted on a wire myograph, no differences were observed in responses to acetylcholine and H₂S donor sodium hydrosulfide between treated and untreated BDL rats. In the liver, PAG treatment significantly reduced the expression of IL-6, TGF-β, and collagen I and markedly attenuated hepatic fibrosis and architectural distortion. Rats treated with PAG also exhibited significantly lower alanine aminotransferase.</p><p><strong>Conclusion: </strong>In BDL rats, inhibition of H₂S synthesis decreases PP and attenuates liver fibrosis, suggesting that targeting H₂S may represent a therapeutic strategy for portal hypertension, potentially through modulation of intrahepatic resistance.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-11"},"PeriodicalIF":1.3,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13368016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147973399","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":"Deletion of Murine Endothelial <italic>Bag3</italic> Alters the Cellular Proteome among Organs of Origin.","authors":"Zoë S Terwilliger, Feifei Li, Ananya Pentakota, Tonya N Zeczycki, Thomas D Green, Makenzie Kolasa, Nancy C Edwards, Matthew P Goldman, Kelsey H Fisher-Wellman, Joseph M McClung","doi":"10.1159/000552442","DOIUrl":"10.1159/000552442","url":null,"abstract":"<p><strong>Introduction: </strong>Bcl-2 associated athanogene 3 (BAG3) is a multifunctional protein with pleiotropic effects in multiple cell types. Despite our knowledge of its role in cardiovascular disease, its specific role in endothelial cells (ECs) is unknown. The purpose of this study was to identify differences in the EC proteome of multiple tissues before and after cell-specific deletion of Bag3. We hypothesized that BAG3 loss would uniquely alter the baseline proteome landscape of ECs in each tissue.</p><p><strong>Methods: </strong>Cdh5(PAC)-CreERT2;Bag3f/f mice received tamoxifen (KO; n = 18) or vehicle (WT; n = 18) and tissues (brain, heart, lung, and peripheral skeletal muscle-SkM) were collected for fluorescence-activated cell sorting of ECs from equal numbers of male and female mice at >22 weeks of age, followed by LC-MS/MS label-free proteomics.</p><p><strong>Results: </strong>Initial comparisons of the WT proteomes between tissues revealed differential abundance of EC proteins (p < 0.05), including 367 brain vs heart; 338 brain vs. lung; 570 brain vs. SkM; 400 heart vs. lung; 104 heart vs. SkM; and 489 lung vs. SkM. Additionally, the EC mitochondrial proteome was unique to each tissue of origin, with significantly (p < 0.05) higher proportions dedicated to complexes I, III, IV, and V, in the heart compared to the other tissues. KO demonstrated the largest effect on SkM ECs, increasing 31 proteins (Mybpc2 Log2FC = 4.81; PFKM Log2FC = 3.02) and decreasing 65 (CDC42 Log2FC = -2.44; Prpf8 Log2FC = -2.24).</p><p><strong>Conclusion: </strong>Overall, these results demonstrate that the EC proteome of different tissues is unique and that the loss of BAG3 in these cells differentially alters a small proportion of the EC-specific proteome.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-19"},"PeriodicalIF":1.3,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13325460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147864363","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":"Hypertension-Induced Retinal Microvascular Remodeling in Women.","authors":"Rohit S Nampoothiry, Nadra Salman, Ricardo Bernardino de Paula, Laena Pernomian, Paul Townsend, Carolyn M Willmore, Nicholas Riccardi, Sarah E Newman-Norlund, Julius Fridriksson, Leonardo Bonilha, Camilla F Wenceslau, Cameron G McCarthy","doi":"10.1159/000552087","DOIUrl":"10.1159/000552087","url":null,"abstract":"<p><strong>Introduction: </strong>Hypertension is a major risk factor for cardiovascular disease, yet its effects on the retinal microvasculature in women, independent of pregnancy and diabetes, remain poorly understood.</p><p><strong>Methods: </strong>We integrated retinal imaging in female participants with structural assessments in hypertensive female mice to evaluate retinal microvascular remodeling.</p><p><strong>Results: </strong>In women, higher systolic blood pressure was associated with reduced retinal arteriolar area and retinal thinning, independent of BMI or glycemic status. Women over age 50 exhibited greater retinal microvascular loss, suggesting age-related susceptibility. After adjusting for age, retinal arteriolar area remained significantly associated with hypertension, whereas venular area and retinal thickness were primarily associated with age. No significant age × hypertension interactions were observed for any outcome. In parallel, hypertensive BPH/2J mice displayed retinal microvascular rarefaction and reduced pericyte coverage compared with normotensive BPN/3J controls.</p><p><strong>Conclusion: </strong>Across species, hypertension induced rarefaction, arteriolar loss, and pericyte depletion, indicating impaired microvascular integrity. These findings support the utility of retinal imaging as a noninvasive biomarker of hypertensive microvascular disease in women.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-7"},"PeriodicalIF":1.3,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13158893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147699079","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":"Expression of Circulating MicroRNA before and after Abdominal Aneurysm Repair.","authors":"Xinji Tan, Daphne Elisabeth Gray, Kerstin Troidl, Till Keller, Thomas Schmitz-Rixen, Kyriakos Oikonomou","doi":"10.1159/000551833","DOIUrl":"10.1159/000551833","url":null,"abstract":"<p><strong>Introduction: </strong>Numerous studies have identified various miRNAs involved in aortic aneurysm pathology. This study investigated circulating miRNAs before and after abdominal aortic aneurysm repair (open surgical repair [OSR] or endovascular aneurysm repair [EVAR]).</p><p><strong>Methods: </strong>In this prospective, non-randomized, two-arm study, all eligible patients who underwent elective surgery from 2019 to 2021 for infrarenal aortic aneurysms were enrolled. Preoperative, postoperative (day 3), and follow-up serum samples (3 and 12 months) were collected. Circulating miR-29b/29c, miR-155, and miR-15a were analyzed using RT-qPCR.</p><p><strong>Results: </strong>A total of 39 patients (87.2% male) were enrolled (Group I: OSR, n = 17; Group II: EVAR, n = 22). There were no significant differences in the expression of circulating miR-155, miR-15a, miR-29b, or miR-29c between Groups I and II during follow-up. However, subgroup analysis showed significantly lower expression of miR-15a in EVAR patients without an endoleak compared to those with an endoleak, as well as in patients undergoing open repair in the early postoperative phase (day 3).</p><p><strong>Conclusion: </strong>Our study found no significant differences in the expression of miR-155, miR-15a, miR-29b, or miR-29c before and after aneurysm repair, regardless of the surgical approach. However, early postoperative expression of miR-15a was significantly lower in EVAR patients without an endoleak, suggesting a potential role for miR-15a in early aortic remodeling following EVAR.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-11"},"PeriodicalIF":1.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13262996/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147592903","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":"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":"42-52"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","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}