Journal of Vascular Research最新文献_第10页

Follicle-Stimulating Hormone Accelerates Atherosclerosis by Activating PI3K/Akt/NF-κB Pathway in Mice with Androgen Deprivation. 促卵泡激素通过激活PI3K/Akt/NF-κB通路加速雄激素剥夺小鼠动脉粥样硬化

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2022-01-01 DOI: 10.1159/000527239

Jingyu Piao, Yifan Yin, Yaru Zhao, Yi Han, Huixia Zhan, Duosheng Luo, Jiao Guo

{"title":"Follicle-Stimulating Hormone Accelerates Atherosclerosis by Activating PI3K/Akt/NF-κB Pathway in Mice with Androgen Deprivation.","authors":"Jingyu Piao, Yifan Yin, Yaru Zhao, Yi Han, Huixia Zhan, Duosheng Luo, Jiao Guo","doi":"10.1159/000527239","DOIUrl":"https://doi.org/10.1159/000527239","url":null,"abstract":"Objective: Follicle-stimulating hormone (FSH) level changes may be another reason for increasing the risk of cardiovascular disease. In this study, we aimed to investigate the role of FSH in atherosclerosis and its underlying mechanism.Methods: ApoE-/- mice were divided into 4 groups, namely, the sham group, bilaterally orchidectomized group, FSH group, and testosterone-only group. Blood lipid and hormone levels were tested, aorta Oil Red O staining; the levels of NF-κB, Akt, eNOS, and FSH receptors in the aorta were measured by Western blotting. Expression of VCAM-1 was detected via Western blotting and immunohistochemical staining. Human umbilical vein endothelial cells (HUVECs) were used to induce endothelial injury model by adding FSH, and the levels of NF-κB, Akt, eNOS, and FSHR were tested in HUVECs.Results: FSH treatment exacerbated atherosclerotic lesions in ApoE-/- mice. Moreover, FSH could promote the expression of VCAM-1 protein in HUVECs, and this effect was possibly mediated by the activation of NF-κB, while NF-κB activation was further enhanced by the activation of the PI3K/Akt/eNOS pathway. FSH failed to activate Akt and NF-κB in the presence of the PI3K inhibitor LY294002 in HUVECs.Conclusion: FSH promoted the development of atherosclerosis by increasing VCAM-1 protein expression via activating PI3K/Akt/NF-κB pathway.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"59 6","pages":"358-368"},"PeriodicalIF":1.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10442754","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: 1

VEGF-Independent Angiogenic Factors: Beyond VEGF/VEGFR2 Signaling. VEGF独立血管生成因子:超越VEGF/VEGFR2信号传导。

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2022-01-01 Epub Date: 2022-02-11 DOI: 10.1159/000521584

Ryoji Eguchi, Jun-Ichi Kawabe, Ichiro Wakabayashi

{"title":"VEGF-Independent Angiogenic Factors: Beyond VEGF/VEGFR2 Signaling.","authors":"Ryoji Eguchi, Jun-Ichi Kawabe, Ichiro Wakabayashi","doi":"10.1159/000521584","DOIUrl":"https://doi.org/10.1159/000521584","url":null,"abstract":"Tumors induce angiogenesis to acquire oxygen and nutrition from their adjacent microenvironment. Tumor angiogenesis has been believed to be induced primarily by the secretion of vascular endothelial growth factor-A (VEGF-A) from various tumors. VEGF-A binds to VEGF receptor 2 (VEGFR2), resulting in subsequent activation of cellular substances regulating cell proliferation, survival, and angiogenesis. Antiangiogenic therapies targeting the VEGF-A/VEGFR2 axis, including bevacizumab and ramucirumab, humanized monoclonal antibodies against VEGF-A and VEGFR2, respectively, have been proposed as a promising strategy aimed at preventing tumor growth, invasion, and metastasis. Phase III clinical trials using bevacizumab and ramucirumab have shown that not all tumor patients benefit from such antiangiogenic agents, and that some patients who initially benefit subsequently become less responsive to these antibodies, suggesting the possible existence of VEGF-independent angiogenic factors. In this review, we focus on VEGF-independent and VEGFR2-dependent tumor angiogenesis, as well as VEGFR2-independent tumor angiogenesis. Additionally, we discuss VEGF-independent angiogenic factors which have been reported in previous studies. Various molecular targeting drugs are currently being evaluated as potential antitumor therapies. We expect that precision medicine will permit the development of innovative antiangiogenic therapies targeting individual angiogenic factors selected on the basis of the genetic screening of tumors.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"59 2","pages":"78-89"},"PeriodicalIF":1.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39619296","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: 13

The Role of ADAMTS-4 in Atherosclerosis and Vessel Wall Abnormalities. ADAMTS-4在动脉粥样硬化和血管壁异常中的作用。

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2022-01-01 Epub Date: 2022-01-20 DOI: 10.1159/000521498

Rudjer Novak, Stela Hrkac, Grgur Salai, Josko Bilandzic, Luka Mitar, Lovorka Grgurevic

{"title":"The Role of ADAMTS-4 in Atherosclerosis and Vessel Wall Abnormalities.","authors":"Rudjer Novak, Stela Hrkac, Grgur Salai, Josko Bilandzic, Luka Mitar, Lovorka Grgurevic","doi":"10.1159/000521498","DOIUrl":"https://doi.org/10.1159/000521498","url":null,"abstract":"Extracellular matrix proteins are regulated by metzincin proteases, like the disintegrin metalloproteinases with thrombospondin motifs (ADAMTS) family members. This review focuses on the emerging role which ADAMTS-4 might play in vascular pathology, which has implications for atherosclerosis and vessel wall abnormalities, as well as for the resulting diseases, such as cardiovascular and cerebrovascular disease, aortic aneurysms, and dissections. Major substrates of ADAMTS-4 are proteoglycans expressed physiologically in smooth muscle cells of blood vessels. Good examples are versican and aggrecan, principal vessel wall proteoglycans that are targeted by ADAMTS-4, driving blood vessel atrophy, which is why this metzincin protease was implicated in the pathophysiology of vascular diseases with an atherosclerotic background. Despite emerging evidence, it is important not to exaggerate the role of ADAMTS-4 as it is likely only a small piece of the complex atherosclerosis puzzle and one that could be functionally redundant due to its high structural similarity to other ADAMTS family members. The therapeutic potential of inhibiting ADAMTS-4 to halt the progression of vascular disease after initialization of treatment is unlikely. However, it is not excluded that it might find a purpose as a biomarker of vascular disease, possibly as an indicator in a larger cytokine panel.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"59 2","pages":"69-77"},"PeriodicalIF":1.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39837539","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: 11

DNA Methylation Profile of the SREBF2 Gene in Human Fetal Aortas. 人胎儿主动脉中SREBF2基因的DNA甲基化谱。

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2022-01-01 Epub Date: 2021-09-14 DOI: 10.1159/000518513

Concetta Schiano, Maria D'Armiento, Monica Franzese, Rossana Castaldo, Gabriele Saccone, Filomena de Nigris, Vincenzo Grimaldi, Andrea Soricelli, Francesco Paolo D'Armiento, Fulvio Zullo, Claudio Napoli

{"title":"DNA Methylation Profile of the SREBF2 Gene in Human Fetal Aortas.","authors":"Concetta Schiano, Maria D'Armiento, Monica Franzese, Rossana Castaldo, Gabriele Saccone, Filomena de Nigris, Vincenzo Grimaldi, Andrea Soricelli, Francesco Paolo D'Armiento, Fulvio Zullo, Claudio Napoli","doi":"10.1159/000518513","DOIUrl":"https://doi.org/10.1159/000518513","url":null,"abstract":"Increasing evidence suggests that maternal cholesterol represents an important risk factor for atherosclerotic disease in offspring already during pregnancy, although the underlying mechanisms have not yet been elucidated. Eighteen human fetal aorta samples were collected from the spontaneously aborted fetuses of normal cholesterolemic and hypercholesterolemic mothers. Maternal total cholesterol levels were assessed during hospitalization. DNA methylation profiling of the whole SREBF2 gene CpG island was performed (p value <0.05). The Mann-Whitney U test was used for comparison between the 2 groups. For the first time, our study revealed that in fetal aortas obtained from hypercholesterolemic mothers, the SREBF2 gene shows 4 significant differentially hypermethylated sites in the 5'UTR-CpG island. This finding indicates that more effective long-term primary cardiovascular prevention programs need to be designed for the offspring of mothers with hypercholesterolemia. Further studies should be conducted to clarify the epigenetic mechanisms underlying the association between early atherogenesis and maternal hypercholesterolemia during pregnancy.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"61-68"},"PeriodicalIF":1.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39427157","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: 2

Recombinant Human Soluble Thrombomodulin Suppresses Arteritis in a Mouse Model of Kawasaki Disease. 重组人可溶性血栓调节蛋白抑制川崎病小鼠动脉炎模型。

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2022-01-01 Epub Date: 2021-12-20 DOI: 10.1159/000520717

Hironobu Nakayama, Hiroyasu Inada, Tatsuya Inukai, Kenta Kondo, Kazuyuki Hirai, Tomonari Tsutsumi, Yoshiyuki Adachi, Noriko Nagi-Miura, Naohito Ohno, Koji Suzuki

{"title":"Recombinant Human Soluble Thrombomodulin Suppresses Arteritis in a Mouse Model of Kawasaki Disease.","authors":"Hironobu Nakayama, Hiroyasu Inada, Tatsuya Inukai, Kenta Kondo, Kazuyuki Hirai, Tomonari Tsutsumi, Yoshiyuki Adachi, Noriko Nagi-Miura, Naohito Ohno, Koji Suzuki","doi":"10.1159/000520717","DOIUrl":"https://doi.org/10.1159/000520717","url":null,"abstract":"Introduction and objective: Kawasaki disease (KD) is associated with diffuse and systemic vasculitis of unknown aetiology and primarily affects infants and children. Intravenous immunoglobulin (IVIG) treatment reduces the risk of developing coronary aneurysms, but some children have IVIG-resistant KD, which increases their risk of developing coronary artery injury. Here, we investigated the effect of recombinant human soluble thrombomodulin (rTM), which has anticoagulant, anti-inflammatory, and cytoprotective properties on the development of coronary arteritis in a mouse model of vasculitis.Methods: An animal model of KD-like vasculitis was created by injecting mice with Candida albicans water-soluble fraction (CAWS). This model was used to investigate the mRNA expression of interleukin (IL)-10, tumour necrosis factor alpha (TNF-α), and tissue factor (TF), in addition to histopathology of heart tissues.Results: rTM treatment significantly reduces cardiac vascular endothelium hypertrophy by 34 days after CAWS treatment. In addition, mRNA expression analysis revealed that rTM administration increased cardiac IL-10 expression until day 27, whereas expression of TNF-α was unaffected. Moreover, in the spleen, rTM treatment restores IL-10 and TF expression to normal levels.Conclusion: These findings suggest that rTM suppresses CAWS-induced vasculitis by upregulating IL-10. Therefore, rTM may be an effective treatment for KD.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"176-188"},"PeriodicalIF":1.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39742292","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

Stromal Vascular Fraction Reverses the Age-Related Impairment in Revascularization following Injury. 基质血管分数逆转损伤后血管重建中与年龄相关的损伤。

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2022-01-01 DOI: 10.1159/000526002

Gabrielle Rowe, David S Heng, Jason E Beare, Nicholas A Hodges, Evan P Tracy, Walter L Murfee, Amanda J LeBlanc

{"title":"Stromal Vascular Fraction Reverses the Age-Related Impairment in Revascularization following Injury.","authors":"Gabrielle Rowe, David S Heng, Jason E Beare, Nicholas A Hodges, Evan P Tracy, Walter L Murfee, Amanda J LeBlanc","doi":"10.1159/000526002","DOIUrl":"https://doi.org/10.1159/000526002","url":null,"abstract":"Adipose-derived stromal vascular fraction (SVF) has emerged as a potential regenerative therapy, but few studies utilize SVF in a setting of advanced age. Additionally, the specific cell population in SVF providing therapeutic benefit is unknown. We hypothesized that aging would alter the composition of cell populations present in SVF and its ability to promote angiogenesis following injury, a mechanism that is T cell-mediated. SVF isolated from young and old Fischer 344 rats was examined with flow cytometry for cell composition. Mesenteric windows from old rats were isolated following exteriorization-induced (EI) hypoxic injury and intravenous injection of one of four cell therapies: (1) SVF from young or (2) old donors, (3) SVF from old donors depleted of or (4) enriched for T cells. Advancing age increased the SVF T-cell population but reduced revascularization following injury. Both young and aged SVF incorporated throughout the host mesenteric microvessels, but only young SVF significantly increased vascular area following EI. This study highlights the effect of donor age on SVF angiogenic efficacy and demonstrates how the ex vivo mesenteric-window model can be used in conjunction with SVF therapy to investigate its contribution to angiogenesis.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"59 6","pages":"343-357"},"PeriodicalIF":1.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9780192/pdf/nihms-1845606.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10536673","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

Erratum. 勘误表。

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2022-01-01 DOI: 10.1159/000526589

引用次数: 0

Smooth Muscle Cell Notch2 Is Not Required for Atherosclerotic Plaque Formation in ApoE Null Mice. ApoE缺失小鼠动脉粥样硬化斑块形成不需要平滑肌细胞Notch2。

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2022-01-01 DOI: 10.1159/000525258

Jessica Davis-Knowlton, Jacqueline E Turner, Anne Harrington, Lucy Liaw

{"title":"Smooth Muscle Cell Notch2 Is Not Required for Atherosclerotic Plaque Formation in ApoE Null Mice.","authors":"Jessica Davis-Knowlton, Jacqueline E Turner, Anne Harrington, Lucy Liaw","doi":"10.1159/000525258","DOIUrl":"https://doi.org/10.1159/000525258","url":null,"abstract":"Introduction: We previously identified Notch2 in smooth muscle cells (SMC) in human atherosclerosis and found that signaling via Notch2 suppressed human SMC proliferation. Thus, we tested whether loss of Notch2 in SMC would alter atherosclerotic plaque progression using a mouse model.Methods: Atherogenesis was examined at the brachiocephalic artery and aortic root in a vascular SMC null (inducible smooth muscle myosin heavy chain Cre) Notch2 strain on the ApoE-/- background. We measured plaque morphology and size, as well as lipid, inflammation, and smooth muscle actin content after Western diet.Results: We generated an inducible SMC Notch2 null on the ApoE-/- background. We observed ∼90% recombination efficiency with no detectable Notch2 in the SMC. Loss of SMC Notch2 did not significantly change plaque size, lipid content, necrotic core, or medial area. However, loss of SMC Notch2 reduced the contractile SMC in brachiocephalic artery lesions and increased inflammatory content in aortic root lesions after 6 weeks of Western diet. These changes were not present with loss of SMC Notch2 after 14 weeks of Western diet.Conclusions: Our data show that loss of SMC Notch2 does not significantly reduce atherosclerotic lesion formation, although in early stages of plaque formation there are changes in SMC and inflammation.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"59 5","pages":"261-274"},"PeriodicalIF":1.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9588530/pdf/nihms-1815853.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9762783","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

Microvessel Density: Integrating Sex-Based Differences and Elevated Cardiovascular Risks in Metabolic Syndrome. 微血管密度:代谢综合征中基于性别的差异和心血管风险升高。

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2022-01-01 Epub Date: 2021-09-14 DOI: 10.1159/000518787

Angelina Wong, Shu Qing Chen, Brayden D Halvorson, Jefferson C Frisbee

{"title":"Microvessel Density: Integrating Sex-Based Differences and Elevated Cardiovascular Risks in Metabolic Syndrome.","authors":"Angelina Wong, Shu Qing Chen, Brayden D Halvorson, Jefferson C Frisbee","doi":"10.1159/000518787","DOIUrl":"https://doi.org/10.1159/000518787","url":null,"abstract":"Metabolic syndrome (MetS) is a complex pathological state consisting of metabolic risk factors such as hypertension, insulin resistance, and obesity. The interconnectivity of cellular pathways within various biological systems suggests that each individual component of MetS may share common pathological sources. Additionally, MetS is closely associated with vasculopathy, including a reduction in microvessel density (MVD) (rarefaction) and elevated risk for various cardiovascular diseases. Microvascular impairments may contribute to perfusion-demand mismatch, where local metabolic needs are insufficiently met due to the lack of nutrient and oxygen supply, thus creating pathological positive-feedback loops and furthering the progression of disease. Sexual dimorphism is evident in these underlying cellular mechanisms, which places males and females at different levels of risk for cardiovascular disease and acute ischemic events. Estrogen exhibits protective effects on the endothelium of pre-menopausal women, while androgens may be antagonistic to cardiovascular health. This review examines MetS and its influences on MVD, as well as sex differences relating to the components of MetS and cardiovascular risk profiles. Finally, translational relevance and interventions are discussed in the context of these sex-based differences.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-15"},"PeriodicalIF":1.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39427161","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: 5

Single-Cell RNA Sequencing Reveals Novel Genes Regulated by Hypoxia in the Lung Vasculature. 单细胞RNA测序揭示肺血管缺氧调控的新基因。

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2022-01-01 DOI: 10.1159/000522340

Shelby Thomas, Sathiyanarayanan Manivannan, Vidu Garg, Brenda Lilly

{"title":"Single-Cell RNA Sequencing Reveals Novel Genes Regulated by Hypoxia in the Lung Vasculature.","authors":"Shelby Thomas, Sathiyanarayanan Manivannan, Vidu Garg, Brenda Lilly","doi":"10.1159/000522340","DOIUrl":"https://doi.org/10.1159/000522340","url":null,"abstract":"Pulmonary arterial hypertension (PAH) is a chronic progressive disease with significant morbidity and mortality. The disease is characterized by vascular remodeling that includes increased muscularization of distal blood vessels and vessel stiffening associated with changes in extracellular matrix deposition. In humans, chronic hypoxia causes PAH, and hypoxia-induced rodent models of PAH have been used for years to study the disease. With the development of single-cell RNA sequencing technology, it is now possible to examine hypoxia-dependent transcriptional changes in vivo at a cell-specific level. In this study, we used single-cell RNA sequencing to compare lungs from wild-type (Wt) mice exposed to hypoxia for 28 days to normoxia-treated control mice. We additionally examined mice deficient for Notch3, a smooth muscle-enriched gene linked to PAH. Data analysis revealed that hypoxia promoted cell number changes in immune and endothelial cell types in the lung, activated the innate immunity pathway, and resulted in specific changes in gene expression in vascular cells. Surprisingly, we found limited differences in lungs from mice deficient for Notch3 compared to Wt controls. These findings provide novel insight into the effects of chronic hypoxia exposure on gene expression and cell phenotypes in vivo and identify unique changes to cells of the vasculature.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"59 3","pages":"163-175"},"PeriodicalIF":1.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9117417/pdf/nihms-1779393.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9484790","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: 1