JVS-vascular sciencePub Date : 2026-01-01Epub Date: 2026-01-18DOI: 10.1016/j.jvssci.2026.100408
Robin Jansen MD , Markus U. Wagenhäuser MD , Tristan Kölsche MD , Cleopatra Papasimos , Pascal Benkert PhD , Jens Kuhle MD , Marc Pawlitzki MD , Lars Masanneck MD , Stefanie Schreiber MD , Julian Caspers MD , Tobias Ruck MD , Ramona Hagler , Malin Stassen , Daniel Weiss MD , Philipp Arndt , Marc Dörner , Joscha Mulorz MD , Sven G. Meuth MD, PhD , Hubert Schelzig MD , John-Ih Lee MD , Michael Gliem MD
{"title":"Serum levels of neurofilament light chain (NfL) and glial fibrillary acid protein (GFAP) in patients with asymptomatic and symptomatic carotid artery stenosis","authors":"Robin Jansen MD , Markus U. Wagenhäuser MD , Tristan Kölsche MD , Cleopatra Papasimos , Pascal Benkert PhD , Jens Kuhle MD , Marc Pawlitzki MD , Lars Masanneck MD , Stefanie Schreiber MD , Julian Caspers MD , Tobias Ruck MD , Ramona Hagler , Malin Stassen , Daniel Weiss MD , Philipp Arndt , Marc Dörner , Joscha Mulorz MD , Sven G. Meuth MD, PhD , Hubert Schelzig MD , John-Ih Lee MD , Michael Gliem MD","doi":"10.1016/j.jvssci.2026.100408","DOIUrl":"10.1016/j.jvssci.2026.100408","url":null,"abstract":"<div><h3>Objective</h3><div>The treatment of carotid artery stenosis (CAS) for stroke prevention is a matter of debate due to conflicting data, missing recent data, and advances in medical treatment options but also in interventional techniques and surgery. Therefore, the establishment of an easily available marker for brain damage might be a key tool in this patient group to guide treatment.</div></div><div><h3>Methods</h3><div>A retrospective cross-sectional study was conducted leveraging a vascular surgery biobank of 95 patients aged 60 to 80 years. Serum neurofilament light chain (sNfL) and serum glial fibrillary acid protein (sGFAP) were evaluated using highly sensitive electrochemiluminescence immunoassays and z-scores. Discriminatory performance was assessed to differentiate between 19 symptomatic and 76 asymptomatic patients with CAS and their correlation with the degree of stenosis according to ultrasound-based North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria.</div></div><div><h3>Results</h3><div>SNfL levels were markedly elevated in symptomatic compared with asymptomatic patients (median 17.4 vs 3.8 pg/mL; <em>P</em> < .001). sNfL robustly discriminated between these patients (area under the curve = 0.83; 95% confidence interval, 0.72-0.94), as did the NfL z-score (area under the curve = 0.83; 95% confidence interval, 0.71-0.95). Interestingly, within the asymptomatic cohort, sNfL levels demonstrated a significant, positive correlation with the degree of stenosis (Spearman's ρ = 0.24; <em>P</em> = .036). Serum levels of SGFAP were also associated with symptomatic status, albeit with a <em>P</em>-value >.05 (0.1 vs 0.1 pg/mL; (<em>P</em> = .057).</div></div><div><h3>Conclusions</h3><div>The study provides evidence of increased sNfL in symptomatic vs asymptomatic CAS and, of note, of ongoing neuronal or glial damage in some patients with clinically asymptomatic CAS, with a positive correlation between sNfL and the degree of CAS. sNfL is a promising and already accessible blood biomarker that may guide therapeutic decisions in this patient population. The role of sGFAP remains elusive and must be evaluated in larger studies.</div></div><div><h3>Clinical Relevance</h3><div>The CREST-2 trial has recently highlighted the high efficacy of intensive medical management in asymptomatic carotid artery stenosis (CAS), making the selection of patients for revascularization increasingly complex. Our study addresses this challenge by evaluating serum neurofilament light chain (sNfL) and serum glial fibrillary acid protein (sGFAP) as an objective biomarker for neuronal injury. Using individualized z-scores, we demonstrate that sNfL effectively differentiates symptomatic status (area under the curve = 0.828) and significantly correlates with the degree of stenosis in asymptomatic cohorts. These results suggest that sNfL can detect subclinical “silent” damage, providing a valuable biological tool to pinpoint high-risk patie","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100408"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147357902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JVS-vascular sciencePub Date : 2026-01-01Epub Date: 2026-02-11DOI: 10.1016/j.jvssci.2026.100412
Linda L. Demer MD, PhD , Yin Tintut PhD
{"title":"Bones of contention: Hematopoietic marrow within the artery wall","authors":"Linda L. Demer MD, PhD , Yin Tintut PhD","doi":"10.1016/j.jvssci.2026.100412","DOIUrl":"10.1016/j.jvssci.2026.100412","url":null,"abstract":"","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100412"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147384834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JVS-vascular sciencePub Date : 2026-01-01Epub Date: 2026-02-11DOI: 10.1016/j.jvssci.2026.100411
Keisuke Kamada MD , Hong Niu PhD , Fan Zhang PhD , Gale L. Tang MD
{"title":"Comparison between vascular smooth muscle cells isolated from descending thoracic and abdominal aortas of mice in cell function, phenotype features, and gene expression","authors":"Keisuke Kamada MD , Hong Niu PhD , Fan Zhang PhD , Gale L. Tang MD","doi":"10.1016/j.jvssci.2026.100411","DOIUrl":"10.1016/j.jvssci.2026.100411","url":null,"abstract":"<div><h3>Background</h3><div>Vascular smooth muscle cells (VSMCs) are the primary component of the medial layer of the vessel wall, where they maintain structural integrity and regulate vascular tone. Their dysfunction contributes to vascular diseases such as aortic aneurysms and atherosclerosis. Although VSMCs isolated from thoracic and abdominal aortic regions are widely used in experimental studies, their functional differences have not been systematically compared.</div></div><div><h3>Methods</h3><div>In this study, we examined functional and phenotypic differences between VSMCs isolated from the descending thoracic (Th-SMCs) and abdominal aortas of male C57BL/6J mice under controlled in vitro conditions.</div></div><div><h3>Results</h3><div>Both cell types maintained high α-smooth muscle actin expression across passages, supporting smooth muscle lineage identity. Functionally, Th-SMCs demonstrated significantly greater migratory and proliferative capacities compared with abdominal SMCs. Under sublethal oxidative stress, Th-SMCs exhibited higher relative viability, accompanied by higher basal expression of antioxidant-related transcripts, including <em>Nrf2</em>, <em>Catalase</em>, and <em>Sod1</em>.</div></div><div><h3>Conclusions</h3><div>These findings highlight intrinsic differences between region-specific VSMCs and underscore the importance of considering anatomical origin for in vitro models. Incorporating region-specific VSMCs may enhance experimental relevance and contribute to a better understanding of the mechanisms underlying regional vascular diseases.</div></div><div><h3>Clinical Relevance</h3><div>Vascular smooth muscle cells (VSMCs) play a key role in the development of vascular diseases. This study demonstrates that VSMCs isolated from the descending thoracic and abdominal aortic regions exhibit distinct functional behaviors under in vitro conditions. These region-specific differences highlight the importance of carefully selecting and reporting the anatomical origin of VSMCs in experimental studies, which may improve the physiological relevance and interpretability of vascular research models.</div></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100411"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147384833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JVS-vascular sciencePub Date : 2026-01-01Epub Date: 2025-11-29DOI: 10.1016/j.jvssci.2025.100399
Yae Hyun Rhee MD , Joshua M. Spin MD, PhD , Philip S. Tsao PhD
{"title":"A narrative review of recent literature of circulating biomarkers of abdominal aortic aneurysm","authors":"Yae Hyun Rhee MD , Joshua M. Spin MD, PhD , Philip S. Tsao PhD","doi":"10.1016/j.jvssci.2025.100399","DOIUrl":"10.1016/j.jvssci.2025.100399","url":null,"abstract":"<div><h3>Objective</h3><div>Abdominal aortic aneurysms (AAAs) arise through complex pathogenesis, and good methods of risk stratification have proved elusive. Further, the lack of medical options short of surgery for treatment, and the requirement for dedicated imaging for identification, result in delayed diagnosis and hamper patient outcomes. Application of circulating biomarkers to effectively assess disease presence and predict progression would improve clinical management and support patient well-being. Exploration for suitable circulating biomarkers of AAAs is still very much in process; however, no disease-specific biomarker has yet been established for effective diagnosis and prognosis. This review aims to contribute enhanced tools for utilizing biomarkers for risk stratification and management of AAA disease.</div></div><div><h3>Methods</h3><div>Utilizing MEDLINE/PubMed, we summarize 44 recent publications covering circulating AAA biomarkers. The biomarkers were categorized and tiered into six subgroups by study design, with prospective studies tiered higher than retrospective observational studies. The classification system separately describes a list of post-interventional monitoring biomarkers. Part of the review also deals with recent approaches to identifying potential AAA biomarkers by genetic inference.</div></div><div><h3>Results</h3><div>Forty individual circulating biomarkers, two plasma protein panels (consisting of 9 or 7 proteins), one plasma-multiomic study, and two micro-RNA (miR) panels revealed correlations to AAA disease risk. Among those, many have already been established as biomarkers for other cardiovascular diseases, meaning feasibility has been proven but disease specificity is lacking.</div></div><div><h3>Conclusions</h3><div>Multiple circulating proteins and miRs have been investigated for their utility as AAA-specific diagnostic or prognostic biomarkers. This work may ultimately identify not only novel AAA biomarkers that are specific for cell type, proteins, metabolites, genetic polymorphisms, and miRNA, but permit framing of comprehensive networks of disease-participating molecules. More robust data with higher disease sensitivity and specificity are needed, along with more multi-centered longitudinal clinical studies with large sample sizes.</div></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100399"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146023639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JVS-vascular sciencePub Date : 2026-01-01Epub Date: 2026-02-24DOI: 10.1016/j.jvssci.2026.100413
William J. Yoon MD, PhD , Andres Schanzer MD , Kevin Mani MD, PhD , Anders Wanhainen MD, PhD
{"title":"Changes in local hemodynamic forces associated with arch branched endografts","authors":"William J. Yoon MD, PhD , Andres Schanzer MD , Kevin Mani MD, PhD , Anders Wanhainen MD, PhD","doi":"10.1016/j.jvssci.2026.100413","DOIUrl":"10.1016/j.jvssci.2026.100413","url":null,"abstract":"<div><h3>Objective</h3><div>Different zone 0 endograft designs have been introduced. This study sought to assess postimplantation hemodynamic changes induced by zone 0 endografts, with varied configuration of side branches, using computational models.</div></div><div><h3>Methods</h3><div>Twenty-nine patients who underwent zone 0 endovascular repair with single-, double-, or triple-branched endografts (n = 7, n = 11, n = 11, respectively), using different configurations of antegrade (A) and retrograde (R) branches, were included. Computational simulations were used to assess postimplantation changes in peak flow rate, systolic blood pressure (SBP) and time-averaged wall shear stress (TAWSS) at the innominate artery (IA), right subclavian artery, right common carotid artery (CCA), left CCA (LCCA), left subclavian artery (LSA), and distal aortic arch, as well as the total displacement force (DF) of the endograft.</div></div><div><h3>Results</h3><div>Regardless of orientation, IA side branch implantation increased the IA peak flow rate across all endograft designs, an effect significant only in single-branched devices (+70%, <em>P</em> = .02). This increase was accompanied by a significant decrease in peak flow in the LCCA and LSA for single- (<em>P</em> = .02 and <em>P</em> = .02, respectively) and double-branched devices (<em>P</em> = .01 and <em>P</em> < .001, respectively), whereas no such effect was observed with triple-branched devices. Notably, the two antegrade branches supplying the IA and LCCA and one retrograde branch to the LSA- and three retrograde branches (3R)-triple-branched designs had the opposite effect on LCCA blood flow (+8.3% vs −6.7% [<em>P</em> = .02], respectively), although their impact on LSA flow did not differ significantly (−7.5% vs −8.1% [<em>P</em> = .92], respectively). This resulted in disparate effects on distal arch flow (−0.3% vs +6.3% [<em>P</em> = .02], respectively). Postimplantation alteration in distal arch flow was progressively attenuated with more branches. The preimplantation to postimplantation SBP differences in the IA, LCCA, and LSA mirrored the corresponding changes in peak flow. Elevated peak flow in the IAs led to a significant postimplantation increase in the TAWSS across all device designs. In contrast, the LSA side branches with retrograde orientation in the two antegrade branches supplying the IA and LCCA and one retrograde branch to the LSA-triple-branched and 3R-triple-branched endografts demonstrated marked increases in TAWSS (36.1% vs 50.2%, respectively), despite there being no significant change in the mean flow rate. Although maximum DF varied between devices (single-branched, 32.8 N; double-branched, 23.9 N; 2A+1-triple-branched, 22.9 N; 3R-triple-branched, 28.9 N), a post hoc analysis showed that branch configuration did not significantly influence DF.</div></div><div><h3>Conclusions</h3><div>The hemodynamic stability within the aortic arch improves with a greater number of endograft","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100413"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147538356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JVS-vascular sciencePub Date : 2026-01-01Epub Date: 2025-12-16DOI: 10.1016/j.jvssci.2025.100404
Camilo Polania Sandoval MD , James F. Meschia MD , Mercedes Prudencio PhD , Tania Gendron PhD , Christopher Jacobs MD , Richard D. Beegle MD , Sukhwinder J.S. Sandhu MD , Kiran K. Mangalaparthi PhD , Jaeyun Sung PhD , Xiaowei Zhao PhD , Aziza Nassar MD, MPH, MBA , Houssam Farres MD , Leonard Petrucelli PhD , Akhilesh Pandey MD, PhD , Young Erben MD
{"title":"Proteomic signatures of carotid plaque vulnerability: Proteolysis, inflammation, metabolic reprogramming, and lipid dysregulation","authors":"Camilo Polania Sandoval MD , James F. Meschia MD , Mercedes Prudencio PhD , Tania Gendron PhD , Christopher Jacobs MD , Richard D. Beegle MD , Sukhwinder J.S. Sandhu MD , Kiran K. Mangalaparthi PhD , Jaeyun Sung PhD , Xiaowei Zhao PhD , Aziza Nassar MD, MPH, MBA , Houssam Farres MD , Leonard Petrucelli PhD , Akhilesh Pandey MD, PhD , Young Erben MD","doi":"10.1016/j.jvssci.2025.100404","DOIUrl":"10.1016/j.jvssci.2025.100404","url":null,"abstract":"<div><h3>Background</h3><div>Carotid plaque vulnerability is a current feature that aids in the decision-making for ischemic stroke risk. Proteomic analysis of plaque tissue can reveal molecular indicators of instability that complement imaging findings. We sought to identify a proteomic signature distinguishing vulnerable from stable carotid plaques in patients undergoing endarterectomy, with the aim of uncovering candidate biomarkers for potential diagnostic and therapeutic targets.</div></div><div><h3>Methods</h3><div>Twenty-eight carotid plaque specimens were collected from 27 patients (including 1 patient with bilateral endarterectomy). Samples were classified as vulnerable (n = 14) or nonvulnerable (n = 14) based on preoperative magnetic resonance angiography with vessel wall imaging. A tandem mass tag-based multiplexing strategy followed by mass spectrometric analysis was used to profile the proteomes of all samples. Normalized and log<sub>2</sub>-transformed protein intensities were compared using two-sample <em>t</em> tests with unequal variances, and <em>P</em> values were adjusted for multiple testing with the Benjamini-Hochberg method to obtain false discovery rate <em>q</em> values. Proteins with a <em>q</em> value of ≤0.25 were designated high-confidence candidates, and those with a <em>P</em> value of <.05 but a <em>q</em> value of >0.25 were considered exploratory.</div></div><div><h3>Results</h3><div>From 3267 proteins identified, 398 reached nominal significance (<em>P</em> < .05). From those, 29 reached at least log<sub>2</sub>(fold-change) of +1, whereas 3 of −1 log<sub>2</sub>(fold change), yielding a total of 32 proteins. Fifteen were significant for a <em>q</em> value ≤0.25. All were upregulated in vulnerable lesions and these included: matrix-degrading enzymes (matrix metalloproteinase [MMP]7, MMP9, MMP1, and ADAM-like decysin-1), neutrophil-derived effectors (azurocidin, cathelicidin antimicrobial peptide, lactotransferrin, and myeloperoxidase), inflammatory regulators (interleukin-1 receptor antagonist and interleukin-4-induced protein), glycolytic enzymes (hexokinase-3 and hexokinase-2), and lipid-handling proteins (lipoprotein-associated phospholipase A<sub>2</sub>, apolipoprotein B, and paraoxonase-1). An additional 17 exploratory proteins showed nominal significance (<em>P</em> < .05, <em>q</em> > 0.25) with at least log<sub>2</sub>(fold-change) of 1, and 366 proteins with nominal significance but with a log<sub>2</sub>(fold-change) of <1.</div></div><div><h3>Conclusions</h3><div>Our proteomic profiling delineates a robust vulnerability signature marked by enhanced proteolysis, neutrophil activation, inflammatory signaling, metabolic reprogramming, and lipid dysregulation. High-confidence proteins emerged as tissue biomarkers of plaque instability. Validating their association with future cerebrovascular events is the next step toward clinically actionable stroke prediction. Exploratory candidates w","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100404"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JVS-vascular sciencePub Date : 2026-01-01Epub Date: 2025-12-17DOI: 10.1016/j.jvssci.2025.100405
Gözde Tekin MD , Özge Çevik PhD , Şule Çetinel MD , Göksel Şener PhD , Mehmet Kızılay MD
{"title":"Montelukast attenuates abdominal aortic aneurysm in rats: Anti-inflammatory and antioxidant effects","authors":"Gözde Tekin MD , Özge Çevik PhD , Şule Çetinel MD , Göksel Şener PhD , Mehmet Kızılay MD","doi":"10.1016/j.jvssci.2025.100405","DOIUrl":"10.1016/j.jvssci.2025.100405","url":null,"abstract":"<div><h3>Objective</h3><div>Oxidative stress and inflammation are widely recognized as central mechanisms in the pathogenesis of abdominal aortic aneurysm. This study sought to examine the potential protective properties of montelukast in a rat model of aortic aneurysm.</div></div><div><h3>Methods</h3><div>Male Sprague-Dawley rats were randomly allocated into three experimental groups. Abdominal aortic aneurysm was induced using the calcium chloride (CaCl<sub>2</sub>) model, in which gauze soaked in 0.5 M CaCl<sub>2</sub> was placed directly onto the adventitial surface of the infrarenal abdominal aorta for 15 minutes. After induction, the treatment group received daily intraperitoneal injections of montelukast (10 mg/kg) for 4 consecutive weeks. At the study end point, animals were euthanized, and infrarenal aortic tissues were harvested for biochemical and histological evaluations. Measured parameters included matrix metalloproteinase (MMP)-2 and MMP-9 expression, myeloperoxidase (MPO) activity, and 8-hydroxy-2′-deoxyguanosine levels. Antioxidant capacity was assessed through superoxide dismutase (SOD) activity assays. Histopathological examinations were performed, and statistical analysis was conducted using GraphPad Prism v.5.</div></div><div><h3>Results</h3><div>Exposure to CaCl<sub>2</sub> triggered pronounced oxidative injury and inflammation, as evidenced by elevated 8-hydroxy-2′-deoxyguanosine levels, increased MPO activity, reduced SOD activity, and upregulated MMP-2 and MMP-9 expression. Montelukast administration markedly attenuated these changes, normalizing oxidative and inflammatory markers while improving histopathological architecture.</div></div><div><h3>Conclusions</h3><div>Montelukast effectively counteracted CaCl<sub>2</sub>-induced aortic damage. The protective effects of montelukast appear to be mediated through suppression of MMP activity, restoration of SOD levels, and reduction of MPO-driven oxidative injury. By mitigating both inflammatory and oxidative mechanisms, montelukast contributes to the preservation of aortic wall structure.</div></div><div><h3>Clinical Relevance</h3><div>Abdominal aortic aneurysm remains a major vascular disorder without an effective pharmacological therapy to slow its progression. In this experimental study, montelukast, a leukotriene receptor antagonist widely used in asthma, attenuated abdominal aortic aneurysm formation in rats and was associated with increased superoxide dismutase activity, reduced myeloperoxidase levels, and suppressed matrix metalloproteinase activation. These combined antioxidant, anti-inflammatory, and matrix-stabilizing effects preserved aortic wall integrity. Given montelukast's established safety and clinical availability, these findings support its potential for future clinical investigation as a pharmacological approach to limit aneurysm progression.</div></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100405"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145927781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JVS-vascular sciencePub Date : 2026-01-01Epub Date: 2025-11-27DOI: 10.1016/j.jvssci.2025.100398
Bowen Wang PhD
{"title":"Adipocyte renin-angiotensin system signaling in periaortic fat: Neutral findings with mechanistic implications","authors":"Bowen Wang PhD","doi":"10.1016/j.jvssci.2025.100398","DOIUrl":"10.1016/j.jvssci.2025.100398","url":null,"abstract":"","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"7 ","pages":"Article 100398"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145927782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}