Journal of Vascular Research最新文献

{"title":"Transcapillary PO2 Gradients in Contracting Muscle of Rat Model of Sepsis.","authors":"Narumi Fukuzaki, Kazuki Hotta, Kota Izawa, Naoki Hitosugi, Miki Sakamoto, Rin Kataoka, Shuri Arai, Kentaro Kamiya, Atsuhiko Matsunaga","doi":"10.1159/000547568","DOIUrl":"https://doi.org/10.1159/000547568","url":null,"abstract":"<p><strong>Objectives: </strong>This study aimed to evaluate the effect of cecal ligation and puncture (CLP)-induced sepsis on transcapillary PO2 gradients (ΔPO2) in contracting skeletal muscle.</p><p><strong>Methods: </strong>Male Wistar rats (n = 16, 10 weeks old) were randomly assigned to sham or CLP groups. Seven days after surgery, microvascular (PO2mv) and interstitial (PO2is) PO2 levels in the tibialis anterior (TA) muscle were measured using the phosphorescence quenching method during the transition from rest to electrically induced muscle contractions. ΔPO2 was calculated as PO2mv minus PO2is.</p><p><strong>Results: </strong>At rest, there were no differences in PO2mv, PO2is, and ΔPO2 between the sham and CLP groups. The PO2mv and PO2is decreased during the transition from rest to contractions in both groups. During muscle contractions, the PO2mv and ΔPO2 were significantly lower in the CLP group than in the sham group (PO2mv, 7.79 ± 5.03 vs. 4.43 ± 2.23; ΔPO2, 5.50 ± 4.46 vs. 1.82 ± 2.66 mmHg; sham vs. CLP; P < 0.05). The ΔPO2 of the rats in the sham group remained unchanged; however, it markedly decreased during muscle contractions in the CLP group.</p><p><strong>Conclusion: </strong>Sepsis reduced transcapillary PO2 gradients in contracting skeletal muscles.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-15"},"PeriodicalIF":1.8,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144707942","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":"Clinical and Coronary Artery Lesion Characteristics and Outcomes in Acute Coronary Syndrome Patients with High Bleeding Risk.","authors":"Nobuaki Kobayashi, Yusaku Shibata, Osamu Kurihara, Shota Shigihara, Tomofumi Sawatani, Akihiro Shirakabe, Masamichi Takano, Kuniya Asai","doi":"10.1159/000547565","DOIUrl":"https://doi.org/10.1159/000547565","url":null,"abstract":"<p><strong>Background: </strong>Although it is well-known that patients with high bleeding risk (HBR) who undergo percutaneous coronary intervention (PCI) have poor clinical outcomes, the details have not been fully clarified for acute coronary syndrome (ACS) population. The aim of this study was to describe patient and lesion characteristics in patients with ACS and HBR as defined by the Academic Research Consortium (ARC).</p><p><strong>Methods: </strong>Patients with ACS (n=961) who underwent optical coherence tomography (OCT)-guided PCI were investigated. They were divided into HBR and non-HBR groups according to the ARC HBR criteria. Clinical background, lesion characteristics on angiography and OCT, and clinical outcomes during the two-year follow-up period were compared between the groups.</p><p><strong>Results: </strong>The HBR group comprised 307 patients (32%). The frequency of multi-vessel coronary disease was higher in the HBR group than the non-HBR group (34% vs. 26%, p=0.015). OCT findings demonstrated a higher frequency of calcified nodules as the underlying pathology for ACS in the HBR group (12% vs. 3%, p<0.001), with a correspondingly higher frequency of calcified plaques (55% vs. 39%, p<0.001). Kaplan-Meier estimates of the incidence of major bleeding (11.0% vs. 2.4%, p<0.001) and cardiac death (8.5% vs. 2.4%, p<0.001) were more prevalent for the HBR group than the non-HBR group during the follow-up period.</p><p><strong>Conclusion: </strong>ACS patients with HBR factors had more advanced atherosclerosis which contributed to a higher prevalence of cardiac death as well as major bleeding complications.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-20"},"PeriodicalIF":1.8,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144707941","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":"AKAP12 variant 1 knockout enhances vascular endothelial cell motility.","authors":"Ashrifa Ali, Bhaskar Roy, Micah B Schott, Bryon D Grove","doi":"10.1159/000547350","DOIUrl":"https://doi.org/10.1159/000547350","url":null,"abstract":"<p><p>This study investigates the role of AKAP12 in endothelial cell motility with a specific focus on AKAP12 variants, AKAP12v1 and AKAP12v2. Previous work has shown that AKAP12, a multivalent A-kinase anchoring protein that binds to PKA and several other proteins regulating protein phosphorylation, is expressed at low levels in most endothelia in vivo but is expressed at higher levels in cells in vitro. Here, we found that AKAP12 expression in endothelial cell (HUVEC) cultures was cell density-dependent, with the expression being highest in subconfluent cultures and lowest in confluent cultures. AKAP12 expression was also elevated in cells at the wound edge of wounded endothelial cell monolayers. Knockdown of variants 1 and 2 inhibited cell migration. However, CRISPR/Cas9 knockout of AKAP12v1 enhanced migration, indicating that the absence of this variant and the presence of AKAP12v2 likely alters the signaling events controlling cell motility. Further analysis using bulk RNA sequencing revealed that the loss of AKAP12v1 affected genes associated with cell migration and intercellular junctions. We propose that AKAP12v1 and AKAP12v2 play distinct yet complementary roles in endothelial cell migration and likely work together in controlling the signaling events associated with vascular repair and development.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-24"},"PeriodicalIF":1.8,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675130","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":"Mitochondria-Targeted SS-31 Conjugated Liposome Attenuate Oxidative Stress in Endothelial and Skeletal Muscle Cells.","authors":"Eun-Mi Kim, Yeon-Hee Han, Phil-Sun Oh, Wang Qi, Seok-Tae Lim, Hwan-Jeong Jeong","doi":"10.1159/000547281","DOIUrl":"https://doi.org/10.1159/000547281","url":null,"abstract":"<p><strong>Background: </strong>Mitochondria play a pivotal role as therapeutic targets in a range of disorders, including metabolic and neurodegenerative diseases. SS31, a peptide engineered to target mitochondria, offers potent antioxidant activity, positioning it as a promising therapeutic option. Nevertheless, the hydrophilic profile of SS31 poses challenges such as reduced stability, suboptimal delivery, and poor mitochondrial localization in clinical applications.</p><p><strong>Aim: </strong>This study was designed to develop a mitochondria-targeted liposomal carrier by conjugating SS31KRKC to the liposome surface (SS31-LP) and to investigate its biological effects in vitro.</p><p><strong>Methods: </strong>A lysine-arginine-lysine-cysteine (KRKC) linker was incorporated with SS31 to facilitate surface conjugation to liposomes via thiol-based coupling. The hydrodynamic diameter and zeta potential of the resulting formulations were quantified to determine the optimal lipid-to-peptide ratio for mitochondrial targeting. The in vitro mitochondrial localization, cytotoxicity, antioxidant potential, and anti-apoptotic efficacy of SS31-LP were evaluated in HUVEC and C2C12 cells.</p><p><strong>Results: </strong>SS31-LP demonstrated pronounced mitochondrial localization and showed variable cellular internalization based on zeta potential. Pretreatment with SS31-LP enhanced cellular viability, mitigated oxidative damage, and reduced apoptosis in response to oxidative stress caused by H₂O₂ or blue LEDs.</p><p><strong>Conclusion: </strong>Overall, SS31-LP presents as a valuable therapeutic strategy for cellular protection against oxidative injury and may be an advantageous platform for targeted drug delivery applications.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-30"},"PeriodicalIF":1.8,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144659540","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":"Erratum.","authors":"","doi":"10.1159/000545807","DOIUrl":"10.1159/000545807","url":null,"abstract":"","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1"},"PeriodicalIF":1.8,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094680/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144120131","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":"Neointimal Smooth Muscle Cells in Mouse Vein Grafts Are Not Recruited from the Adjacent Artery.","authors":"Klas Österberg, Joakim Håkansson, Erney Mattsson","doi":"10.1159/000546237","DOIUrl":"10.1159/000546237","url":null,"abstract":"<p><strong>Introduction: </strong>Smooth muscle cells (SMCs) with an origin separate from the local vein wall contribute to formation of intimal hyperplasia (IH) in mouse vein grafts. The recruitment pathway of these cells has not been defined, but circulating progenitor cells and cells from the surrounding tissue or adjacent artery to which the vein graft is anastomosed are potential sources. The aim of this study was to clarify if cells from the adjacent artery contribute to neointimal formation in vein grafts.</p><p><strong>Methods: </strong>Aortic segments from donor SM22α-LacZ mice were anastomosed to vein segments from wild-type (WT) C57BL/6 mice ex vivo followed by implantation of the composite grafts to the right common carotid arteries of WT recipient mice. Six weeks after surgery, the composite grafts were harvested, and histology was analyzed in longitudinal sections. SMCs with origin in the SM22α-LacZ arterial segments were identified with X-gal staining.</p><p><strong>Results: </strong>LacZ-positive cells were found in the medial layer of the SM22α-LacZ arterial segments but were not found in the IH in the vein graft segment.</p><p><strong>Conclusion: </strong>SMCs in vein grafts are not recruited from the adjacent artery through migration across the anastomosis.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-8"},"PeriodicalIF":1.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12121965/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144002357","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":"Heat Therapy as a Viable Treatment for Peripheral Artery Disease: A Mini Review.","authors":"Min-Hyeok Jang, Song-Young Park, Sun Dong Kim, Sang Ho Lee","doi":"10.1159/000546163","DOIUrl":"10.1159/000546163","url":null,"abstract":"<p><strong>Background: </strong>Peripheral artery disease (PAD) is a prevalent and debilitating condition characterized by reduced blood flow to the lower limb extremities due to arterial plaque buildup. Traditional exercise/walking therapies have been used to improve vascular function and walking performance but suffer from low adherence rates due to pain and discomfort. Heat therapy has emerged as a promising alternative, showing similar improvements in vascular and cardiovascular function, often with higher adherence rates.</p><p><strong>Summary: </strong>This review explores various forms of heat therapy, including passive and active modalities, and their effects on patients with PAD. Heat therapies have demonstrated similar or even superior outcomes compared to traditional exercise/walking therapies, with higher adherence rates.</p><p><strong>Key messages: </strong>Despite promising results, further research is needed to standardize heat therapy protocol and understand the underlying mechanisms. Optimizing heat therapy could offer a viable, patient-friendly alternative to improve vascular function, reduce pain, and enhance quality of life in patients with PAD.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-13"},"PeriodicalIF":1.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033250","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":"The Functional Unit of the Lymphatic System: Towards Understanding the Importance of a Well-Rehearsed Interaction of Lymphatic Capillaries, Collecting Vessels, and Lymph Nodes.","authors":"Katrin Sabine Roth, Reinhard Pabst","doi":"10.1159/000545084","DOIUrl":"10.1159/000545084","url":null,"abstract":"<p><strong>Introduction: </strong>Lymphatic vessels and lymph nodes (LNs) are part of the lymphatic system taking care of interstitial tissue homoeostasis, lipid transport, and immune response. The interposition of LNs in between the lymphatic vasculature allows the filtration of lymph fluid, cell-cell interactions, and also the transfer of lymph fluid into the venous system. An important role of lymphatic flow, which is often underestimated, is the active involvement of lymph flow and the lymphatic vasculature in immunologic function.</p><p><strong>Summary: </strong>The present review summarizes the current knowledge of the different functional units of the lymphatic transport system trying to create a model of their interplay and options to react to inflammatory conditions. Remodelling of the lymphatic system during inflammation includes lymphangiogenesis, changed fluid transport rates, and modification of LN morphology. Alterations of these processes can aggravate inflammatory processes, leading to an incomplete resolution of the inflammation and often ending in chronic inflammatory condition. Despite the development of histological markers to visualize lymphatic vessels, new imaging methods and increased knowledge about the different parts of the lymphatic system the general overview about the interplay of the different components is missing.</p><p><strong>Key messages: </strong>We show the importance of lymphatic flow in the initiation of the immune response and the solution of an inflammation. We speculate that the increase in density and vessel diameter of lymph vessels is necessary to increase the fluid influx, efflux and the migration of cells into the LN. A failure of antigen-tissue clearance leads to chronic inflammation. Remodelling of LN morphology and vasculature is also necessary in this reaction. An overrun of the defending capacity of the LN is prevented by the immune system via control of the lymph vessel transport capacity and LN remodelling.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-10"},"PeriodicalIF":1.8,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657612","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":"Unstable Coronary Artery Plaque Features in Humans Are Associated with Higher Frequency of Circulating CD56bright Natural Killer Cells.","authors":"Micah Hunter-Chang, Christine L Flora, Hema Kothari, Chantel C McSkimming, Sydney D Blimbaum, Corey M Williams, Angela M Taylor, Stefan Bekiranov, Coleen A McNamara","doi":"10.1159/000544884","DOIUrl":"10.1159/000544884","url":null,"abstract":"<p><strong>Introduction: </strong>Unstable human artery plaques can suddenly rupture, leading to MI or stroke. Identification of blood markers associated with unstable plaque features is clearly needed. Humans with symptomatic carotid atherosclerotic plaques have increased infiltration of CD56bright natural killer (NK) cells into the plaque, yet whether subjects with unstable coronary artery plaque features have increased frequencies of circulating CD56bright NK cells is unknown.</p><p><strong>Methods: </strong>Coronary artery intravascular ultrasound (IVUS) was performed on subjects presenting for medically indicated coronary angiography. Eighteen subjects stratified into high and low percent (%) necrotic core and matched for age, body mass index (BMI), and lipids underwent mass cytometry by time-of-flight analysis on their peripheral blood mononuclear cells collected prior to imaging. Clustering of major immune cell populations was performed on live singlets and CD56 bright and dim NK subsets were quantitated.</p><p><strong>Results: </strong>Subjects with high necrotic core had a significantly greater frequency of circulating CD56bright NK cells compared to subjects with low necrotic core (p = 0.02). Additionally, the frequency of circulating CD56bright NK cells positively associated with IVUS-VH metrics of total atheroma volume (p = 0.0013), percent (%) atheroma burden (p = 0.0048), % maximum stenosis (p = 0.0021), % necrotic (p = 0.0013), % calcium (p = 0.0016), % fatty (p = 0.0097) and negatively associated with % fibrous (p < 0.0001), an IVUS-VH metric of plaque stability.</p><p><strong>Conclusion: </strong>These findings suggest that the frequency of CD56bright NK cells may be a safe, noninvasive marker of plaque volume and instability.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-7"},"PeriodicalIF":1.8,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542523","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":"Single Intraluminal Delivery of a Nitric Oxide-Donor Results in Inhibition of Intimal Thickening in the Rabbit Femoral Artery.","authors":"Priyanka Böttger, Tilo Grosser, Waltraut Ibe, Jean-Paul Boissel, Stephan Lindemann, Karl Werdan, HansJörg Schwertz, Harald Darius, Michael Buerke","doi":"10.1159/000544029","DOIUrl":"10.1159/000544029","url":null,"abstract":"<p><strong>Introduction: </strong>Vascular smooth muscle cell (SMC) proliferation and vascular homeostasis are thought to be regulated by nitric oxide and prostaglandins. The loss of these endogenous mediators seems to play an important role for the development of restenosis following balloon angioplasty.</p><p><strong>Methods: </strong>We examined the effect of exogenous linsidomine, a nitric oxide (NO) releasing compound, in a model of balloon injury iliac arteries of rabbits. On the cellular levels, NO can exert effects like cell survival, growth, and proliferation inhibition, has effects on transcription and proteasome effects and mitochondria-related effects in SMCs. SMC proliferation was quantified as a change of intima-media ratio. Linsidomine injection or its vehicle was performed with an infusion-balloon catheter directly into the dilated vessel wall.</p><p><strong>Results: </strong>Balloon angioplasty resulted in a significant increase of intima-media ratio during the first 3 weeks. Linsidomine treatment decreased the intima-media ratio significantly compared to vehicle treated animals 3 weeks after balloon angioplasty (0.65 ± 0.05 vs 1.2 ± 0.2 intima-media ratio, p < 0.05). However, control vessels had an intima-media ratio of 0.15 ± 0.02. This effect was similar to NOS-2 transfected vessels following angioplasty. Immunohistochemical analysis demonstrated the expression of the proliferating cellular nuclear antigen in dilated vessel of vehicle treated animals, which was reduced in linsidomine-treated rabbits. In in vitro experiments, linsidomine inhibited significantly and dose-dependently rabbit SMC proliferation measured by BrdU incorporation. Further linsidomine increased rate of apoptotic SMCs, however, this effect was p53 independent.</p><p><strong>Conclusion: </strong>Simultaneous angioplasty of the rabbit iliac artery and direct injection of linsidomine into the vessel wall seem to be an effective strategy to reduce neointima formation. Similar, local application of liposome encapsulation of human nitric oxide synthase-2 transfection resulted in potent inhibition of intima proliferation and SMC proliferation due to local restoration NO within the injured vasculature.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-11"},"PeriodicalIF":1.8,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189633","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}