Journal of Vascular Research最新文献_第4页

Basic Characteristics of Systemic Arteries of Different Organs. 不同器官全身动脉的基本特征。

IF 1.3 4区医学

Journal of Vascular Research Pub Date : 2026-01-01 Epub Date: 2026-02-23 DOI: 10.1159/000551138

Anastasia A Shvetsova, Olga A Vlaskina, Sofia D Kabiolskaya, Ilya A Kabiolsky, Dina K Gaynullina

{"title":"Basic Characteristics of Systemic Arteries of Different Organs.","authors":"Anastasia A Shvetsova, Olga A Vlaskina, Sofia D Kabiolskaya, Ilya A Kabiolsky, Dina K Gaynullina","doi":"10.1159/000551138","DOIUrl":"10.1159/000551138","url":null,"abstract":"Introduction: The vessels of different organs may demonstrate functional heterogeneity depending on organ they supply. However, few works systematically examine arteries of different organs. We hypothesized that arteries of different organs will demonstrate different passive pressure-diameter responses and functional responses to contractile and dilatory agonists.Methods: Mesenteric, sural, interlobar renal, basilar, and septal coronary arteries of Wistar rats were studied using wire myography.Results: Sural and coronary arteries had a slightly smaller diameter compared to other studied vessels. Passive elastic characteristics of the studied vessels were similar. Only sural and basilar arteries tended to develop considerable stretch-induced tone. Mesenteric, sural, and renal arteries demonstrated similar maximum contractile response to agonist of α1-adrenoceptors methoxamine, while mesenteric arteries showed the lowest sensitivity to this agonist. The maximum contractile response and sensitivity of basilar artery to thromboxane A2 analog U46619 were higher compared to coronary arteries. The smallest amplitude of maximum relaxation to acetylcholine was found for renal artery.Conclusion: Our data demonstrate that even general characteristics of arteries like stretch-induced tone, sensitivity to contractile and dilatory agonists vary between the arteries of comparable caliber, but from different organs.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"222-230"},"PeriodicalIF":1.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147276622","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}

引用次数: 0

Immunosuppression Drugs Exhibit Differential Effects on Endothelial Cell Function. 免疫抑制药物对内皮细胞功能的不同影响

IF 1.3 4区医学

Journal of Vascular Research Pub Date : 2026-01-01 Epub Date: 2025-09-11 DOI: 10.1159/000548353

Aly Elezaby, Ryan Dexheimer, David Wu, Sze Yu Chan, Ines Ross Tacco, Ian Y Chen, Nazish Sayed, Karim Sallam

{"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":"Introduction: 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.Methods: We utilized induced pluripotent stem cell-derived endothelial cells to investigate the role of widely used immunosuppression drugs on endothelial cell function.Results: We found that among immunosuppression agents, sirolimus reduced basic endothelial cell functions including cell migration, proliferation, acetylated LDL uptake, mitochondrial respiration, and angiogenic properties, while tacrolimus only reduced nitric oxide release.Conclusions: This model allows for investigation of differential effect of immunosuppression drugs on endothelial function that can elucidate the mechanisms contributing to clinically observed adverse vascular profiles.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-13"},"PeriodicalIF":1.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12772628/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effect of Water Temperature during Aquatic Exercise on Cognitive Impairment in Mice with Chronic Cerebral Hypoperfusion. 水中运动水温对慢性脑灌注不足小鼠认知功能损害的影响。

IF 1.3 4区医学

Journal of Vascular Research Pub Date : 2026-01-01 Epub Date: 2025-12-16 DOI: 10.1159/000550096

Chiyeon Lim, Sehyun Lim, Sung Min Moon, Suin Cho

{"title":"Effect of Water Temperature during Aquatic Exercise on Cognitive Impairment in Mice with Chronic Cerebral Hypoperfusion.","authors":"Chiyeon Lim, Sehyun Lim, Sung Min Moon, Suin Cho","doi":"10.1159/000550096","DOIUrl":"10.1159/000550096","url":null,"abstract":"Introduction: Given the lack of effective pharmacotherapy for vascular dementia (VaD) and the reported benefits of exercise, this study examined the impact of water temperature during aquatic exercise (AE) on cognitive and pathological outcomes in a mouse model of VaD.Methods: Twelve-month-old male mice underwent bilateral common carotid artery stenosis (BCAS) to induce chronic cerebral hypoperfusion. Groups included sham, BCAS control (no exercise), and BCAS mice assigned to AE in water baths at 25°C, 30°C, or 35°C. Cognitive performance was assessed using the elevated plus maze, Y-maze, and novel object recognition test (NORT). Brain tissues were analyzed for microglial marker CD68, astrocytic marker GFAP, and myelin basic protein (MBP) in the corpus callosum.Results: The 30°C AE group showed the greatest improvement in NORT performance and swim activity. CD68 expression was unchanged across groups, but GFAP expression was significantly reduced at 30°C, suggesting suppressed astrocyte activation. Furthermore, the decline in MBP expression after BCAS was attenuated in this group, indicating preserved white matter integrity.Conclusion: AE at approximately 30°C alleviated cognitive deficits in a VaD model, likely by reducing neuroinflammation and protecting myelin. These findings highlight the therapeutic potential of optimizing AE conditions, particularly water temperature, for dementia-related rehabilitation. .","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"120-134"},"PeriodicalIF":1.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12845522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145768657","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}

引用次数: 0

Differential Blood-Brain Barrier Permeability Driven by Asymmetric Hypoperfusion in a Vascular Dementia Model. 血管性痴呆模型中不对称低灌注驱动的不同血脑屏障通透性。

IF 1.3 4区医学

Journal of Vascular Research Pub Date : 2026-01-01 Epub Date: 2026-01-16 DOI: 10.1159/000548796

Mengjun Dai, Kuizhi Qu, Ying Jiang, Song Gao, Yan-Ning Rui, Zhen Xu

{"title":"Differential Blood-Brain Barrier Permeability Driven by Asymmetric Hypoperfusion in a Vascular Dementia Model.","authors":"Mengjun Dai, Kuizhi Qu, Ying Jiang, Song Gao, Yan-Ning Rui, Zhen Xu","doi":"10.1159/000548796","DOIUrl":"10.1159/000548796","url":null,"abstract":"Introduction: Blood-brain barrier (BBB) dysfunction has been associated with vascular dementia (VaD). However, the underlying mechanisms causing BBB dysfunction remain unclear, especially regarding cerebral hypoperfusion. This study aimed to investigate the effects of asymmetric hypoperfusion on BBB permeability using a mouse model of VaD.Methods: Asymmetric bilateral common carotid artery stenosis (ACAS) was induced using ligature rings. BBB integrity was assessed on 3 days post-surgery using Evans blue, IgG, and albumin extravasation. A modified tissue processing protocol optimized endogenous marker detection. Regional and sex-based differences in BBB permeability were analyzed.Results: Increased BBB permeability was observed in both corpus callosum and cortical areas, with significantly more severe leakage in the left cortex compared to the right, correlating directly with lower cerebral blood flow on the left side. In contrast, no significant asymmetrical difference in BBB permeability was detected in the corpus callosum. Additionally, male and female mice exhibited similar patterns of BBB permeability.Conclusion: This study provides the first evidence that asymmetrical hypoperfusion significantly impacts regional BBB permeability in a mouse model of VaD. These findings highlight the importance of local hemodynamic changes in driving BBB dysfunction and underscore potential therapeutic targets for preventing or mitigating VaD progression.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"135-145"},"PeriodicalIF":1.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13023342/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145989758","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}

引用次数: 0

Plasmin-PAI-1 Imbalance Contributes to Hyperglycemia-Induced Vascular Calcification. 纤溶蛋白pai -1失衡有助于高血糖诱导的血管钙化。

IF 1.3 4区医学

Journal of Vascular Research Pub Date : 2026-01-01 Epub Date: 2026-03-14 DOI: 10.1159/000551570

Yosuke Kanno, Moeko Okuno, Osamu Matsuo, Kei-Ichi Ozaki

{"title":"Plasmin-PAI-1 Imbalance Contributes to Hyperglycemia-Induced Vascular Calcification.","authors":"Yosuke Kanno, Moeko Okuno, Osamu Matsuo, Kei-Ichi Ozaki","doi":"10.1159/000551570","DOIUrl":"10.1159/000551570","url":null,"abstract":"Introduction: Vascular calcification (VC) is a frequent complication in diabetes and is linked to an increased risk of thrombotic cardiovascular events. Diabetes is characterized by impaired fibrinolysis, and accumulating evidence implicates fibrin deposition in VC progression. However, how fibrinolytic dysregulation contributes to VC remains unclear.Methods: We examined the role of fibrinolytic factors in VC using an established in vitro model. Vascular smooth muscle cells were cultured under high glucose conditions to evaluate glucose-induced VC and plasminogen activator inhibitor-1 (PAI-1) expression. In addition, exogenous plasmin stimulation was performed to assess its effects on VC progression and anti-calcific signaling.Results: High glucose enhanced VC and markedly increased PAI-1 expression. Inhibition of PAI-1 signaling attenuated glucose-induced VC, indicating its involvement in VC development under hyperglycemia. Conversely, exogenous plasmin reduced VC under normoglycemic conditions. Short-term plasmin stimulation activated AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS), both known inhibitors of VC.Conclusion: These findings suggest that PAI-1 contributes to hyperglycemia-related VC, whereas plasmin exerts protective effects partly through AMPK-eNOS activation. Modulating plasmin activity or targeting PAI-1 may represent potential therapeutic approaches to prevent VC progression in diabetes.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"244-254"},"PeriodicalIF":1.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147457350","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}

引用次数: 0

Deficiency of p27^kip1, a Cyclin-Dependent Kinase Inhibitor, Accelerates Topical Elastase/3-Aminopropionitrile Fumarate Salt-Induced Abdominal Aortic Aneurysm Development in Mice. 细胞周期蛋白依赖性激酶抑制剂p27kip1的缺乏会加速外用弹性蛋白酶/3-氨基丙腈富马酸盐诱导的小鼠腹主动脉瘤的发展。

IF 1.3 4区医学

Journal of Vascular Research Pub Date : 2026-01-01 Epub Date: 2025-09-04 DOI: 10.1159/000547829

Keisuke Kamada, Hong Niu, Shinsuke Kikuchi, Nobuyoshi Azuma, Gale L Tang

{"title":"Deficiency of p27kip1, 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":"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.Methods: 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.Results: 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.Conclusion: 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. .","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"29-41"},"PeriodicalIF":1.3,"publicationDate":"2026-01-01","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}

引用次数: 0

Hydroxychloroquine Administration Mitigates Atherosclerotic Plaque Progression in ApoE Knockout Mice by Inhibiting Neutrophil Extracellular Trap Formation and Autophagy. 羟氯喹通过抑制中性粒细胞胞外陷阱的形成和自噬来减轻ApoE基因敲除小鼠动脉粥样硬化斑块的进展。

IF 1.3 4区医学

Journal of Vascular Research Pub Date : 2026-01-01 Epub Date: 2026-03-09 DOI: 10.1159/000550061

Dimitrios Sagris, Anastasia-Maria Natsi, Konstantina Zacharouli, Eleni Banakou, Erietta Polychronopoulou, Irene Poulakida, Evgenios Eftalitsidis, Maria Koffa, Panagiotis Skendros, Konstantinos Ritis, Maria Ioannou, Spiros Georgopoulos, George N Dalekos, Konstantinos P Makaritsis

{"title":"Hydroxychloroquine Administration Mitigates Atherosclerotic Plaque Progression in ApoE Knockout Mice by Inhibiting Neutrophil Extracellular Trap Formation and Autophagy.","authors":"Dimitrios Sagris, Anastasia-Maria Natsi, Konstantina Zacharouli, Eleni Banakou, Erietta Polychronopoulou, Irene Poulakida, Evgenios Eftalitsidis, Maria Koffa, Panagiotis Skendros, Konstantinos Ritis, Maria Ioannou, Spiros Georgopoulos, George N Dalekos, Konstantinos P Makaritsis","doi":"10.1159/000550061","DOIUrl":"10.1159/000550061","url":null,"abstract":"Introduction: Hydroxychloroquine (HCQ) has been associated with lower incidence of cardiovascular events in patients with autoimmune diseases and atherosclerosis progression in mouse models. Our study aimed at investigating the effect of HCQ on autophagy and neutrophil extracellular trap (NET) formation in aortas of ApoE-/- mice.Methods: ApoE-/- mice were treated with 10 mg/kg/day HCQ for 16 weeks. The aortas were examined histologically, while immunofluorescence staining and confocal microscopy were performed to identify the co-localization of myeloperoxidase (MPO) with DNA or microtubule-associated protein 1A/1B-light chain 3B (LC3B) as markers of NET formation and autophagy, respectively.Results: Among 52 ApoE-/- mice (30 male, 22 female), HCQ was administered in 15 male and 12 female mice. HCQ was associated with a significant reduction of the mean (±SD) surface of the atherosclerotic plaque compared to controls (HCQ-treated vs. control, 0.04 ± 0.01 mm2 vs. 0.08 ± 0.04 mm2, p < 0.01 and 0.06 ± 0.04 mm2 vs. 0.15 ± 0.09 mm2, p = 0.012, for male and female, respectively). This reduction was associated with a significant attenuation in the mean fluorescence intensity of MPO and LC3B expression in the atherosclerotic plaque of HCQ-treated mice (p = 0.03 and p = 0.01, respectively). In line with these findings, HCQ significantly reduced the proportion of MPO+ and LC3B+ cells within the atherosclerotic lesions.Conclusions: HCQ administration in ApoE-/- mice may mitigate the progression of atherosclerotic plaque, by inhibiting autophagy and NET formation.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"214-221"},"PeriodicalIF":1.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147390447","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}

引用次数: 0

Cardiometabolic Syndromes and Associated Cardiovascular Risks: A Narrative Review. 心血管代谢综合征和相关心血管风险：叙述性综述。

IF 1.3 4区医学

Journal of Vascular Research Pub Date : 2026-01-01 Epub Date: 2026-02-12 DOI: 10.1159/000549775

Antonio Ruiz-Saavedra, Fernando Vidal-Ostos De Lara, J Alfredo Martínez

{"title":"Cardiometabolic Syndromes and Associated Cardiovascular Risks: A Narrative Review.","authors":"Antonio Ruiz-Saavedra, Fernando Vidal-Ostos De Lara, J Alfredo Martínez","doi":"10.1159/000549775","DOIUrl":"10.1159/000549775","url":null,"abstract":"Background: Cardiovascular risk (CVR) is closely linked to metabolic and endocrine disorders that share common mechanisms such as insulin resistance, adipose tissue dysfunction, low-grade inflammation, and lipid abnormalities. Conditions including metabolic syndrome (MetS), hypertriglyceridemic waist (HTGW), metabolic dysfunction-associated steatotic liver disease (MASLD), cardiorenometabolic (CKM) syndrome, and polycystic ovary syndrome (PCOS) present overlapping yet distinct phenotypes that contribute to vascular injury and cardiometabolic progression.Summary: This review integrates current evidence connecting MetS, HTGW, MASLD, CKM syndrome, and PCOS within a unified cardiometabolic framework. Although each condition has specific diagnostic criteria, they converge pathophysiologically and collectively increase long-term CVR. Understanding these shared pathways may enhance early detection of subclinical disease. Precision medicine strategies incorporating clinical, biochemical, and imaging biomarkers offer the potential for personalised risk stratification and targeted interventions.Key messages: MetS, HTGW, MASLD, CKM syndrome, and PCOS share core mechanisms driving cardiometabolic deterioration. MASLD is a major independent predictor of cardiovascular morbidity and mortality. CKM syndrome represents a continuum integrating metabolic, renal, and cardiovascular dysfunction. Early identification of high-risk phenotypes may improve prevention strategies. Precision medicine approaches can refine CV risk assessment and guide personalised management.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"179-200"},"PeriodicalIF":1.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146180770","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}

引用次数: 0

Unstable Coronary Artery Plaque Features in Humans Are Associated with Higher Frequency of Circulating CD56bright Natural Killer Cells. 人类不稳定的冠状动脉斑块特征与循环CD56bright自然杀伤细胞的高频率相关。

IF 2.3 4区医学

Journal of Vascular Research Pub Date : 2025-01-01 Epub Date: 2025-03-03 DOI: 10.1159/000544884

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

{"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":"Introduction: 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.Methods: 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.Results: 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.Conclusion: These findings suggest that the frequency of CD56bright NK cells may be a safe, noninvasive marker of plaque volume and instability.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"204-210"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12324973/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neointimal Smooth Muscle Cells in Mouse Vein Grafts Are Not Recruited from the Adjacent Artery. 小鼠静脉移植物中的新生内膜平滑肌细胞不是来自邻近动脉。

IF 2.3 4区医学

Journal of Vascular Research Pub Date : 2025-01-01 Epub Date: 2025-05-05 DOI: 10.1159/000546237

Klas Österberg, Joakim Håkansson, Erney Mattsson

{"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":"Introduction: 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.Methods: 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.Results: 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.Conclusion: SMCs in vein grafts are not recruited from the adjacent artery through migration across the anastomosis.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"211-218"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","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}

引用次数: 0