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Mechanism of vascular endothelial growth factor on the prevention of restenosis after angioplasty

Qigong LIU, Honglian ZHOU, Yan ZENG, Shan YE, Jiani LIU, Zaiying LU

《医学前沿（英文）》 2009年 第3卷 第2期   页码 177-180 doi: 10.1007/s11684-009-0021-x

摘要： To evaluate the mechanism of vascular endothelial growth factor (VEGF) on the prevention of restenosis after angioplasty, the recombinant adenovirus vector containing hVEGF cDNA was constructed and transfected into vascular smooth muscle cells (VSMC) . The conditioned medium containing VEGF was collected 72 h after the infection. Then, the VSMC and human umbilical vein endothelial cells (HUVEC) were divided into control group, H O -treated group and H O +VEGF-treated group to observe the proliferation and apoptosis by water soluble tetrazolium (WST-1) method, nick end labeling (TUNEL) and flow cytometry (FCM). Compared with the control and H O +VEGF-treated groups, the absorbance ( ) value of HUVEC was decreased, and apoptosis of HUVEC was significantly increased in H O -treated group. The changes of value and apoptosis of VSMC were contrary to those of HUVEC. H O could stimulate the proliferation of VSMC and induce the apoptosis of HUVEC, inhibit the proliferation of HUVEC and the apoptosis of VSMC and induce restenosis. VEGF could inhibit the effect of H O on HUVEC and VSMC and prevent restenosis. These results offered further theoretical evidence for VEGF on the prevention of restenosis after angioplasty.

关键词： vascular endothelial growth factors     restenosis     reactive oxygen species     endothelial cells     vascular smooth muscle cell    

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Role of nitric oxide in biological effects of vascular endothelial growth factor

Qigong LIU M D , Yan ZENG , Jiani LIU , Shan YE , Yongdong LI , Zaiying LU M D ,

《医学前沿（英文）》 2009年 第3卷 第3期   页码 284-286 doi: 10.1007/s11684-009-0062-1

摘要： To evaluate the role of nitric oxide in the biological effects of vascular endothelial growth factor (VEGF) and the possible mechanism of VEGF, the cultured vascular endothelial cells of rabbit aorta were divided into control group, VEGF-treated group and VEGF+ -nitro-L-arginine methyl ester (L-NAME)-treated group. The absorbance () value of vascular endothelial cells and the levels of prostaglandin (PGI), endothelin-1 (ET-1) and von Willebrand factor (vWF) in the supernatant were observed by water-soluble tetrazolium salt assay, radioimmunoassay and enzyme-linked immunosorbent assay. The values and PGI in VEGF-treated group and VEGF+L-NAME-treated group were higher than those in control group (<0.05 and <0.01). The ET-1 and vWF were significantly decreased in VEGF-treated group and VEGF+L-NAME-treated group compared with the control (<0.05 and <0.01). These results indicate that VEGF could promote the proliferation and secretion of PGI and inhibit the secretion of ET-1 and vWF in vascular endothelial cells and that L-NAME could inhibit the effect of VEGF partially. Nitric oxide is an important mediator in the process of stimulating proliferation and regulating secretion of vascular endothelial cells by VEGF.

关键词： vascular endothelial growth factor     nitric oxide     N-nitro-L-arginine methyl ester     vascular endothelial cells    

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糖尿病发作后心脏脂蛋白脂肪酶的变化 Review

Chae Syng Lee, Yajie Zhai, Brian Rodrigues

《工程（英文）》 2023年 第20卷 第1期   页码 19-25 doi: 10.1016/j.eng.2022.06.013

摘要：

由于心脏持续地收缩和舒张，需要大量的能量，其中脂肪酸（FA）是其三磷酸腺苷（ATP）的主要来源。但是，心脏无法制造这种底物，而是从多种来源获得脂肪酸，包括通过脂蛋白脂肪酶（LPL）的作用。脂蛋白脂肪酶在心肌细胞中产生，随后分泌到质膜上的硫酸乙酰肝素蛋白聚糖（HSPG）结合位点。然后为了将脂蛋白脂肪酶转移到内皮细胞管腔，糖基磷脂酰肌醇锚定的高密度脂蛋白结合蛋白1（GPIHBP1）与间质性脂蛋白脂肪酶结合，并将其转移到血管管腔，在那里脂蛋白脂肪酶可将循环中的甘油三酯分解为脂肪酸。内源性-β-葡萄糖醛酸酶乙酰肝素酶（Hpa）的独特之处在于，它是唯一已知的哺乳动物酶，可以裂解硫酸乙酰肝素，从而促进上述脂蛋白脂肪酶从心肌细胞HSPG中释放。在糖尿病中，一直认为心脏产生能量方式的改变是导致糖尿病性心肌病（DCM）的原因。糖尿病发展到中度后，随着葡萄糖利用率的降低，由于Hpa 作用的增强，心脏血管腔内的脂蛋白脂肪酶活性得到增强。虽然这种适应可能有助于补偿心脏对葡萄糖的利用不足，但从长期来看，它是具有毒性的，因为有害的脂质代谢物积聚，以及脂肪酸氧化增强和因此造成的氧化应激，最终导致细胞死亡。这与一种心脏保护生长因子——血管内皮生长因子B（VEGFB）的丧失同时发生。本文探讨了乙酰肝素酶、脂蛋白脂肪酶和血管内皮生长因子B之间的相互联系及其在糖尿病性心肌病中的潜在影响。鉴于缺乏基于机制的DCM治疗，了解这种心肌病的病理，以及脂蛋白脂肪酶的作用，将有助于我们推进其临床治疗。

关键词： 心脏代谢     脂蛋白脂肪酶     乙酰肝素酶     血管内皮生长因子     糖尿病性心肌病    

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Economic Growth Model Based on Six Basic Factors of Production—Xu Growth Rate Equation

Shou-bo Xu,Zong-yuan Huang

《工程管理前沿（英文）》 2014年 第1卷 第2期   页码 160-175 doi: 10.15302/J-FEM-2014024

摘要： This paper proposes an economic growth model based on the Six Basic Factors of Production and Xu Growth Rate Equation for the first time, which fills-in the deficits of the New Classical Economic Growth Model based on the Solow Model. The empirical analysis indicates that over the past three decades, the consumption of six basic factors of production had complicated relations with economic growth. In some years, the consumption rate of the basic factors of production was meager, but the economy witnessed relatively rocketing growth rate; in some years, the factors of production consumption rate was very high, but the economy growth rate slowed down. In general, economy grows at the expenses of huge consumption of four factors. There is an obvious characteristic of huge input and low efficiency. The average contribution rate of technological advance peaks in the middle, while it drops down at two ends. Noticeably, since 2004, the technology contribution rate generally shows a downward trend, reasons of which should be explored systematically in aspects like economic policy and industry structure with a view to boost further transformation of the macro-economy scientific growth model.

关键词： six basic factors of production     economic growth model     Xu Growth Rate Equation    

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Stroke prevention: an update

null

《医学前沿（英文）》 2012年 第6卷 第1期   页码 22-34 doi: 10.1007/s11684-012-0178-6

摘要：

Stroke is a personal, familial, and social disaster. It is the third cause of death worldwide, the first cause of acquired disability, the second cause of dementia, and its cost is astronomic. The burden of stroke is likely to increase given the aging of the population and the growing incidence of many vascular risk factors. Prevention of stroke includes—as for all other diseases—a “mass approach” aiming at decreasing the risk at the society level and an individual approach, aiming at reducing the risk in a given subject. The mass approach is primarily based on the identification and treatment of vascular risk factors and, if possible, in the implementation of protective factors. These measures are the basis of primary prevention but most of them have now been shown to be also effective in secondary prevention. The individual approach combines a vascular risk factor modification and various treatments addressing the specific subtypes of stroke, such as antiplatelet drugs for the prevention of cerebral infarction in large and small artery diseases of the brain, carotid endarterectomy or stenting for tight carotid artery stenosis, and oral anticoagulants for the prevention of cardiac emboli. There is a growing awareness of the huge evidence-to-practice gap that exists in stroke prevention largely due to socio-economic factors. Recent approaches include low cost intervention packages to reduce blood pressure and cheap “polypills” combining in a single tablet aspirin and several drugs to lower blood pressure and cholesterol. Polypill intake should however not lead to abandon the healthy life-style measures which remain the mainstay of stroke prevention.

关键词： stroke     prevention     vascular risk factors     cerebral infarction     cerebral hemorrhage     anti-thrombotic drugs     carotid endarterectomy    

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Lymphatic metastasis is related to the epithelial-mesenchymal transition and expressions of VEGF, MMP-9, and COX-2 in breast cancer

Lihui WANG, Lianhong LI, Shen LV, Shujun FAN, Li ZHAN, Bo WANG, Zhong ZHANG

《医学前沿（英文）》 2009年 第3卷 第2期   页码 164-170 doi: 10.1007/s11684-009-0038-1

摘要： The invasion and metastasis of breast cancer are supposed to involve several stages in which epithelial-mesenchymal transition (EMT) is regarded as the mechanistic basis for the behavior of cancer cells. A series of factors related to EMT are apparently involved in such process. The current study aimed to investigate the contributions of EMT and related factors in lymph node metastasis of breast cancer. The expressions of E-cadherin (E-Cad), N-cadherin (N-Cad), vascular endothelial cell growth factor (VEGF), matrix metalloproteinase-9 (MMP-9), cyclooxygenase-2 (COX-2), and CD34 were examined in 74 cases of breast cancer, including 39 cases with lymph node metastasis and 35 cases without lymph node metastasis by immunohistochemistry. Multivariable Cox proportional hazards model was used to analyze the patients’ prognosis. The expressions of N-Cad, VEGF, MMP-9, and COX-2 in cases with lymph node metastasis were significantly higher than those without lymph node metastasis ( <0.05), while the E-Cad level was inversely related to status of lymph node metastasis ( <0.05). The metastasis rate of lymph node in the cases with EMT (lower E-Cad expression and higher N-Cad expression) was 78.3%, while that without EMT (higher E-Cad expression and lower N-Cad expression) was 11.1%. There was a statistical difference in the expression of COX-2 protein between histological grade I and grade II or III, respectively ( <0.05). In the cases with higher grade, the expression of E-Cad was decreased, while that of N-Cad was increased. Higher microvascular density (MVD) was also found to be significantly associated with lymphatic metastasis ( <0.05), and the cases with higher MVD had shorter survival time. This study indicates that EMT and expressions of VEGF, MMP-9 and COX-2, and MVD value are strongly correlated with lymph node metastasis in breast cancer.

关键词： epithelial-mesenchymal transition     vascular endothelial cell growth factor     matrix metalloproteinase-9     cyclooxygenase-2     higher microvascular density     breast cancer    

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Effects of resistin on insulin signaling in endothelial cells

Zhizhen LI, Fangping LI, Jianhong YE, Li YAN, Zuzhi FU

《医学前沿（英文）》 2009年 第3卷 第2期   页码 136-140 doi: 10.1007/s11684-009-0029-2

摘要： The objective of this study was to investigate the effects of resistin on insulin signaling in human umbilical vein endothelial cells (HUVECs). HUVECs were incubated with recombinant human resistin (0-100 ng/mL) for 24 h. Akt and endothelial nitric oxide synthase (eNOS) phosphorylation levels of endothelial cells under basal or insulin stimulated conditions were measured by Western blot. Nitric oxide (NO) production of HUVECs was also detected. The results showed that resistin could significantly inhibit Akt and eNOS phosphorylation and NO production in endothelial cells under insulin stimulated conditions ( < 0.05 control). But under basal conditions, treatment with resistin could result in a decrease in eNOS phosphorylation ( < 0.05 control) but had no effect on NO production and Akt phosphorylation levels. These findings suggested that resistin exerted an inhibitory effect on NO production by inhibiting insulin signaling and eNOS phosphorylation in endothelial cells.

关键词： resistin     endothelium     nitric oxide     endothelial nitric oxide synthase     Akt-binding protein     mouse    

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Factors affecting the formation of zeolite seed layers and the effects of seed layers on the growth of

ZHANG Xiongfu, WANG Jinqu, LIU Hai′ou, WANG Anjie

《化学科学与工程前沿（英文）》 2007年 第1卷 第2期   页码 172-177 doi: 10.1007/s11705-007-0032-6

摘要： The present study investigates the formation of silicalite-1 seed layers on a porous carbon support of 0.5 μm pore size and α-A1O supports with different pore sizes (0.1 μm and 4 μm) via the slip-casting technique. The effects of support property, seed size and solvent on the formation of seed layers were investigated in detail. The growth of silicalite-1 membranes on different seeded supports by hydrothermal synthesis was also evaluated. The scanning electron microscopy (SEM) and X-ray diffraction (XRD) characterizations indicate that a continuous seed layer can be obtained on the smooth support of 0.1 μm pore size by using any seed of 100 nm, 600 nm or 2.2 μm in size, whereas, on the coarse supports with either 0.5 μm or 4 μm pore size, a continuous seed layer cannot be formed using the above seed sizes and the same seeding time. At a longer contact time, a seed layer can also be formed using 100 nm seed on the supports with larger pore size. However, the layer is not uniform and smooth. For a hydrophobic porous carbon support, seeding ethanol suspension, which has weak polarity, favors the formation of a continuous seed layer. The seed layers and membranes grown from the smaller seed are more uniform and continuous and possess smoother surfaces than those from the larger seed. The seed layer and respective grown membrane formed from nanosized seed (100 nm) are the most uniform and compact. With this method of seeded secondary synthesis of zeolite membranes, the quality of a membrane mainly depends on the quality of the seed layer.

关键词： silicalite-1     α-A1O     growth     seeding ethanol     quality    

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Emerging roles of podoplanin in vascular development and homeostasis

null

《医学前沿（英文）》 2015年 第9卷 第4期   页码 421-430 doi: 10.1007/s11684-015-0424-9

摘要：

Podoplanin (PDPN) is a mucin-type O-glycoprotein expressed in diverse cell types, such as lymphatic endothelial cells (LECs) in the vascular system and fibroblastic reticular cells (FRCs) in lymph nodes. PDPN on LECs or FRCs activates CLEC-2 in platelets, triggering platelet activation and/or aggregation through downstream signaling events, including activation of Syk kinase. This mechanism is required to initiate and maintain separation of blood and lymphatic vessels and to stabilize high endothelial venule integrity within lymph nodes. In the vascular system, normal expression of PDPN at the LEC surface requires transcriptional activation of Pdpn by Prox1 and modification of PDPN with core 1-derived O-glycans. This review provides a comprehensive overview of the roles of PDPN in vascular development and lymphoid organ maintenance and discusses the mechanisms that regulate PDPN expression related to its function.

关键词： podoplanin     CLEC-2     Prox1     O-glycosylation     lymphatic vascular development and maintenance     lymphoid organ homeostasis    

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Effect of hyperlipidemia on endothelial VCAM-1 expression and the protective role of fenofibrate

WU Jun, LIN Jinchao, HE Zhaochu, OU Biru, GUO Haisen

《医学前沿（英文）》 2007年 第1卷 第4期   页码 356-358 doi: 10.1007/s11684-007-0068-5

摘要： The effect of hyperlipidemia and inflammation on endothelial functions was studied. The enrolled included control (basic chow), hyperlipidemia and fenofibrate-treated groups (high fat diet). The hyperlipidemia model was set up by four-week atherogenic diet, followed by a 16-week treatment in the fenofibrate-treated group (fenofibrate 40 mg/kg every day) and without treatment in the hyperlipidemia group, respectively. In the 20th week, serum lipid level and NO levels were measured, and the expression of vascular cell adhesion molecule-1 (VCAM-1) and cell adhesiveness in aortic endothelia observed by computer-aided system. Compared with the control group, hyperlipidemia rats showed lower levels of NO and ncreases in leukocyte accumulation on the endothelial surface, also stronger and more extensive endothelial expression of VCAM-1. In fenofibrate-treated group, the expression of VCAM-1 and leukocyte accumulation on the endothelial surface was decreased, while serum levels of NO were increased as compared with hyperli pidemia group. Hyperlipidemia can inhibit the NO activity and promote the damage of VACA-1 to aortic endothelia. Fenofibrate can effectively prevent the pathogenesis of atherosclerosis by restoring NO levels and down-regulating the VCAM-1 expression.

关键词： endothelial     16-week treatment     leukocyte accumulation     mg/kg     NO    

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Endothelial dysfunction in COVID-19 calls for immediate attention: the emerging roles of the endothelium

Weijian Hang, Chen Chen, Xin A. Zhang, Dao Wen Wang

《医学前沿（英文）》 2021年 第15卷 第4期   页码 638-643 doi: 10.1007/s11684-021-0831-z

摘要： The COVID-19 pandemic has caused numerous deaths around the world. A growing body of evidence points to the important role of overwhelming inflammatory responses in the pathogenesis of COVID-19 and the effectiveness of anti-inflammation therapy against COVID-19 is emerging. In addition to affecting the lungs, COVID-19 can be a severe systemic inflammatory disease that is related to endothelial dysfunction. We are calling for closer attention to endothelial dysfunction in COVID-19 not only for fully revealing the pathogenic mechanism of COVID-19 but also for properly adjusting the strategy of clinical intervention.

关键词： COVID-19     endothelial dysfunction     inflammation reaction     cytokine storm    

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Crk-associated substrate, vascular smooth muscle and hypertension

TANG Dale

《医学前沿（英文）》 2008年 第2卷 第4期   页码 323-331 doi: 10.1007/s11684-008-0062-6

摘要： Hypertension is characterized by vascular smooth muscle constriction and vascular remodeling involving cell migration, hypertrophy and growth. Crk-associated substrate (CAS), the first discovered member of the adapter protein CAS family, has been shown to be a critical cellular component that regulates various smooth muscle functions. In this review, the molecular structure and protein interactions of the CAS family members are summarized. Evidence for the role of CAS in the regulation of vascular smooth muscle contractility is presented. Contraction stimulation induces CAS phosphorylation on Tyr-410 in arterial smooth muscle, creating the binding site for the Src homology (SH) 2/SH3 protein CrkII, which activates neuronal Wiskott-Aldrich syndrome protein (N-WASP)-mediated actin assembly and force development. The functions of CAS in cell migration, hypertrophy and growth are also summarized. Abelson tyrosine kinase (Abl), c-Src, focal adhesion kinase (FAK), proline-rich tyrosine kinase 2 (PYK2), protein tyrosine phosphatase-proline, glutamate, serine and threonine sequence protein (PTP-PEST) and SHP-2 have been documented to coordinate the phosphorylation and dephosphorylation of CAS. The downstream signaling partners of CAS in the context of cell motility, hypertrophy, survival and growth are also discussed. These new findings establish the important role of CAS in the modulation of vascular smooth muscle functions. Furthermore, the upstream regulators of CAS may be new biologic targets for the development of more effective and specific treatment of cardiovascular diseases such as hypertension.

关键词： Contraction stimulation     phosphatase-proline     molecular structure     discovered     hypertension    

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Study on the action of resistin-induced human umbilical vein endothelial cell dysfunction

LI Zhizhen, LI Fangping, YAN Li, LI Feng, LI Yan, CHENG Hua, FU Zuzhi

《医学前沿（英文）》 2007年 第1卷 第2期   页码 196-199 doi: 10.1007/s11684-007-0037-z

摘要： The aim of this paper was to investigate the effects of resistin on human umbilical vein endothelial cells (HUVECs), and to explore its role and mechanism of action in atherosclerosis. HUVECs were incubated with recombinant human resistin (0, 50, 100 ng/mL) for 24 h. ICAM-1, VCAM-1 and reactive oxygen species (ROS) were assayed by flow cytometer. ET-1, eNOS and iNOS mRNA expression were measured by semi-quantitative RT-PCR. Incubation of HUVECs with resistin resulted in an increase in ICAM-1 expression and ET-1 mRNA expression. However, resistin had no effect on VCAM-1 expression and ROS release. eNOS and iNOS mRNA expression were not altered by resistin stimulation. Adipokine resistin exerted a direct effect in promoting HUVEC dysfunction by promoting ICAM-1 and ET-1 expression. These data suggest that adipocyteendothelium cross-talk might play an important role in the pathogenesis of cardiovascular disease in diabetes mellitus.

关键词： endothelial     resistin stimulation     Incubation     pathogenesis     dysfunction    

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lncR-GAS5 upregulates the splicing factor to impair endothelial autophagy, leading to atherogenesis

《医学前沿（英文）》 2023年 第17卷 第2期   页码 317-329 doi: 10.1007/s11684-022-0931-4

摘要： Long noncoding RNAs (lncRNAs) play a critical role in the regulation of atherosclerosis. Here, we investigated the role of the lncRNA growth arrest-specific 5 (lncR-GAS5) in atherogenesis. We found that the enforced expression of lncR-GAS5 contributed to the development of atherosclerosis, which presented as increased plaque size and reduced collagen content. Moreover, impaired autophagy was observed, as shown by a decreased LC3II/LC3I protein ratio and an elevated P62 level in lncR-GAS5-overexpressing human aortic endothelial cells. By contrast, lncR-GAS5 knockdown promoted autophagy. Moreover, serine/arginine-rich splicing factor 10 (SRSF10) knockdown increased the LC3II/LC3I ratio and decreased the P62 level, thus enhancing the formation of autophagic vacuoles, autolysosomes, and autophagosomes. Mechanistically, lncR-GAS5 regulated the downstream splicing factor SRSF10 to impair autophagy in the endothelium, which was reversed by the knockdown of SRSF10. Further results revealed that overexpression of the lncR-GAS5-targeted gene miR-193-5p promoted autophagy and autophagic vacuole accumulation by repressing its direct target gene, SRSF10. Notably, miR-193-5p overexpression decreased plaque size and increased collagen content. Altogether, these findings demonstrate that lncR-GAS5 partially contributes to atherogenesis and plaque instability by impairing endothelial autophagy. In conclusion, lncR-GAS5 overexpression arrested endothelial autophagy through the miR-193-5p/SRSF10 signaling pathway. Thus, miR-193-5p/SRSF10 may serve as a novel treatment target for atherosclerosis.

关键词： lncR-GAS5     miR-193-5p     splicing factor SRSF10     autophagy     atherogenesis    

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Progress in tumor vascular normalization for anticancer therapy: challenges and perspectives

null

《医学前沿（英文）》 2012年 第6卷 第1期   页码 67-78 doi: 10.1007/s11684-012-0176-8

摘要：

Antitumor angiogenic therapy has been shown promising in the treatment of several advanced cancers since the approval of the first antiangiogenic drug Avastin in 2004. Although the current antiangiogenic drugs reduce the density of tumor blood vessels and result in tumor shrinkage at the early stage of treatment, recent studies have shown that antiangiogenic therapy has transient and insufficient efficacy, resulting in tumor recurrence in patients after several months of treatment. Blockage of blood and oxygen supplies creates a hypoxic and acidic microenvironment in the tumor tissues, which fosters tumor cells to become more aggressive and metastatic. In 2001, Jain proposed tumor vascular normalization as an alternative approach to treating cancers based on the pioneering work on tumor blood vessels by several other researchers. At present, normalizing the disorganized tumor vasculature, rather than disrupting or blocking them, has emerged as a new option for anticancer therapy. Preclinical and clinical data have shown that tumor vascular normalization using monoclonal antibodies, proteins, peptides, small molecules, and pericytes resulted in decreased tumor size and reduced metastasis. However, current tumor vascular normalizing drugs display moderate anticancer efficacy. Accumulated data have shown that a variety of vasculogenic/angiogenic tumor cells and genes play important roles in tumor neovascularization, growth, and metastasis. Therefore, multiple-targeting of vasculogenic tumor cells and genes may improve the efficacy of tumor vascular normalization. To this end, the combination of antiangiogenic drugs with tumor vascular normalizing therapeutics, as well as the integration of Western medicine with traditional Chinese medicine, may provide a good opportunity for discovering novel tumor vascular normalizing drugs for an effective anticancer therapy.

关键词： angiogenesis     vasculogenesis     neovascularization     tumor     vasculature     normalization     traditional Chinese medicine    

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标题 作者 时间 类型 操作

Mechanism of vascular endothelial growth factor on the prevention of restenosis after angioplasty

Qigong LIU, Honglian ZHOU, Yan ZENG, Shan YE, Jiani LIU, Zaiying LU

期刊论文

Role of nitric oxide in biological effects of vascular endothelial growth factor

Qigong LIU M D , Yan ZENG , Jiani LIU , Shan YE , Yongdong LI , Zaiying LU M D ,

期刊论文

糖尿病发作后心脏脂蛋白脂肪酶的变化

Chae Syng Lee, Yajie Zhai, Brian Rodrigues

期刊论文

Economic Growth Model Based on Six Basic Factors of Production—Xu Growth Rate Equation

Shou-bo Xu,Zong-yuan Huang

期刊论文

Stroke prevention: an update

null

期刊论文

Lymphatic metastasis is related to the epithelial-mesenchymal transition and expressions of VEGF, MMP-9, and COX-2 in breast cancer

Lihui WANG, Lianhong LI, Shen LV, Shujun FAN, Li ZHAN, Bo WANG, Zhong ZHANG

期刊论文

Effects of resistin on insulin signaling in endothelial cells

Zhizhen LI, Fangping LI, Jianhong YE, Li YAN, Zuzhi FU

期刊论文

Factors affecting the formation of zeolite seed layers and the effects of seed layers on the growth of

ZHANG Xiongfu, WANG Jinqu, LIU Hai′ou, WANG Anjie

期刊论文

Emerging roles of podoplanin in vascular development and homeostasis

null

期刊论文

Effect of hyperlipidemia on endothelial VCAM-1 expression and the protective role of fenofibrate

WU Jun, LIN Jinchao, HE Zhaochu, OU Biru, GUO Haisen

期刊论文

Endothelial dysfunction in COVID-19 calls for immediate attention: the emerging roles of the endothelium

Weijian Hang, Chen Chen, Xin A. Zhang, Dao Wen Wang

期刊论文

Crk-associated substrate, vascular smooth muscle and hypertension

TANG Dale

期刊论文

Study on the action of resistin-induced human umbilical vein endothelial cell dysfunction

LI Zhizhen, LI Fangping, YAN Li, LI Feng, LI Yan, CHENG Hua, FU Zuzhi

期刊论文

lncR-GAS5 upregulates the splicing factor to impair endothelial autophagy, leading to atherogenesis

期刊论文

Progress in tumor vascular normalization for anticancer therapy: challenges and perspectives

null

期刊论文