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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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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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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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New definition of metabolic dysfunction-associated fatty liver disease with elevated brachial-ankle pulse

《医学前沿（英文）》 2022年 第16卷 第5期   页码 714-722 doi: 10.1007/s11684-021-0888-8

摘要： A new definition of metabolic dysfunction-associated fatty liver disease (MAFLD) has recently been proposed. We aim to examine the associations of MAFLD, particularly its discordance from non-alcoholic fatty liver disease (NAFLD), with the progression of elevated brachial-ankle pulse wave velocity (baPWV) and albuminuria in a community-based study sample in Shanghai, China. After 4.3 years of follow-up, 778 participants developed elevated baPWV and 499 developed albuminuria. In comparison with the non-MAFLD group, the multivariable adjusted odds ratio (OR) of MAFLD group for new-onset elevated baPWV was 1.25 (95% confidence interval (CI) 1.01–1.55) and 1.35 (95% CI 1.07–1.70) for albuminuria. Participants without NAFLD but diagnosed according to MAFLD definition were associated with higher risk of incident albuminuria (OR 1.77; 95% CI 1.07–2.94). Patients with MAFLD with high value of hepamet fibrosis score or poor-controlled diabetes had higher risk of elevated baPWV or albuminuria. In conclusion, MAFLD was associated with new-onset elevated baPWV and albuminuria independently of body mass index, waist circumference, and hip circumference. Individuals without NAFLD but diagnosed as MAFLD had high risk of albuminuria, supporting that MAFLD criteria would be practical for the evaluation of long-term risk of subclinical atherosclerosis among fatty liver patients.

关键词： metabolic dysfunction-associated fatty liver disease     non-alcoholic fatty liver disease     fibrosis score     brachial-ankle pulse wave velocity     albuminuria    

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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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Berberine alleviates myocardial diastolic dysfunction by modulating Drp1-mediated mitochondrial fission

《医学前沿（英文）》 doi: 10.1007/s11684-023-0983-0

摘要： Berberine alleviates myocardial diastolic dysfunction by modulating Drp1-mediated mitochondrial fission and Ca homeostasis in a murine model of HFpEF

关键词： mitochondrial fission Ca     Berberine alleviates myocardial     murine model HFpEF    

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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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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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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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Relationship of endothelial nitric oxide synthase gene polymorphism with blood pressure, lipid profile

TANG Zhongzhi, LI Junyao, YANG Jianhong

《医学前沿（英文）》 2008年 第2卷 第2期   页码 178-181 doi: 10.1007/s11684-008-0033-y

摘要： To study the relationship of the polymorphism of endothelial nitric oxide synthase (eNOS) gene and blood pressure, lipid profiles and blood glucose level. By using PCR-RFLP, the eNOS Glu298Asp gene polymorphism was detected in 184 patients with essential hypertension and 196 matched healthy individuals with normal blood pressure. Taking into account eNOS Glu298Asp polymorphisms, the relationship of blood pressure with triglycerides (TG), total cholesterol (TC), high density lipoprotein (HDL), low density lipoprotein (LDL) and blood glucose level was analyzed. The distribution of eNOS Glu298Asp polymorphism had no significant difference between different blood pressure groups and gender groups, but there was a significant difference between different age groups, diastolic blood pressure groups or BMI groups ( < 0.05). Asp/Asp genotype significantly increased the risk of hypertension in individuals with serum TC above 5.4 mmol/L ( = 0.03, = 2.65). eNOS Glu298Asp polymorphism and serum lipid could synergistically modulate the blood pressure. eNOS Asp/Asp genotype could significantly increase the risk of hypertension in individuals with serum TC over 5.4 mmol/L. eNOS Glu298Asp in combination with serum TC could be used to predict the risk of hypertension.
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CD176 single-chain variable antibody fragment inhibits the adhesion of cancer cells to endothelial cells

null

《医学前沿（英文）》 2016年 第10卷 第2期   页码 204-211 doi: 10.1007/s11684-016-0443-1

摘要：

CD176 (Thomsen-Friedenreich antigen) is a tumor-associated carbohydrate epitope (glycotope) functionally involved in blood spread and liver metastasis of cancer cells by mediating the adhesion of cancer cells to endothelial cells and hepatocytes, respectively. CD176 could be a promising target for antitumor immunotherapy. We applied B lymphocytes obtained from mice immunized with CD176 antigen and constructed a phage display library. A positive clone of CD176 single-chain variable antibody fragment (scFv) was successfully screened from this library. The CD176 scFv was expressed in Escherichia coli and purified. The purified scFv can bind to the natural CD176 expressed on the surface of cancer cells. Furthermore, the CD176 scFv inhibits the adhesion of CD176+ cancer cells to endothelial cells and hepatocytes. This CD176 scFv provides a basis for future development of recombinant CD176-specific antibodies that can be used in therapeutic application.

关键词： CD176     Thomsen-Friedenreich antigen     scFv     cancer     therapy     adhesion     metastasis    

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Prognostic value of fasting glucose on the risk of heart failure and left ventricular systolic dysfunction

Hui Wang, Yang Zhang, Zhujun Shen, Ligang Fang, Zhenyu Liu, Shuyang Zhang

《医学前沿（英文）》 2021年 第15卷 第1期   页码 70-78 doi: 10.1007/s11684-020-0749-x

摘要： Recent studies have shown that acute blood glucose elevation in patients with ST-segment elevation myocardial infarction (STEMI) suggests a poor prognosis. To investigate the effect of fasting blood glucose (FBG) on the risk of heart failure (HF) and left ventricular systolic dysfunction (LVSD) in non-diabetic patients undergoing primary percutaneous coronary intervention (PCI) for acute STEMI, we retrospectively recruited consecutive non-diabetic patients who underwent primary PCI for STEMI in our hospital from February 2003 to March 2015. The patients were divided into two groups according to the FBG level. A total of 623 patients were recruited with an age of 61.3±12.9 years, of whom 514 (82.5%) were male. The HF risk (odds ratio 3.401, 95% confidence interval (CI) 2.144–5.395, <0.001) was significantly increased in patients with elevated FBG than those with normal FBG. Elevated FBG was also independently related to LVSD (β 1.513, 95%CI 1.282–1.785, <0.001) in a multiple logistics regression analysis. In conclusion, elevated FBG was independently associated with 30-day HF and LVSD risk in non-diabetic patients undergoing primary PCI for STEMI.

关键词： myocardial infarction     percutaneous coronary intervention     diabetes mellitus     fasting glucose     heart failure    

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Clinical characteristics and risk factors of COVID-19 patients with chronic hepatitis B: a multi-center retrospective cohort study

《医学前沿（英文）》 2022年 第16卷 第1期   页码 111-125 doi: 10.1007/s11684-021-0854-5

摘要： The coronavirus disease 2019 (COVID-19) has spread globally. Although mixed liver impairment has been reported in COVID-19 patients, the association of liver injury caused by specific subtype especially chronic hepatitis B (CHB) with COVID-19 has not been elucidated. In this multi-center, retrospective, and observational cohort study, 109 CHB and 327 non-CHB patients with COVID-19 were propensity score matched at an approximate ratio of 3:1 on the basis of age, sex, and comorbidities. Demographic characteristics, laboratory examinations, disease severity, and clinical outcomes were compared. Furthermore, univariable and multivariable logistic and Cox regression models were used to explore the risk factors for disease severity and mortality, respectively. A higher proportion of CHB patients (30 of 109 (27.52%)) developed into severe status than non-CHB patients (17 of 327 (5.20%)). In addition to previously reported liver impairment markers, such as alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and total bilirubin, we identified several novel risk factors including elevated lactate dehydrogenase (≥245 U/L, hazard ratio (HR) = 8.639, 95% confidence interval (CI) = 2.528–29.523; P <0.001) and coagulation-related biomarker D-dimer (≥0.5 μg/mL, HR= 4.321, 95% CI= 1.443–12.939; P = 0.009) and decreased albumin (<35 g/L, HR= 0.131, 95% CI= 0.048–0.361; P <0.001) and albumin/globulin ratio (<1.5, HR= 0.123, 95% CI= 0.017–0.918; P = 0.041). In conclusion, COVID-19 patients with CHB were more likely to develop into severe illness and die. The risk factors that we identified may be helpful for early clinical surveillance of critical progression.

关键词： COVID-19     chronic hepatitis B     liver injury     coagulation dysfunction    

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Haploinsufficiency of Lipin3 leads to hypertriglyceridemia and obesity by disrupting the expression and nucleocytoplasmic localization of Lipin1

《医学前沿（英文）》 doi: 10.1007/s11684-023-1003-0

摘要： Lipin proteins including Lipin 1–3 act as transcriptional co-activators and phosphatidic acid phosphohydrolase enzymes, which play crucial roles in lipid metabolism. However, little is known about the function of Lipin3 in triglyceride (TG) metabolism. Here, we identified a novel mutation (NM_001301860: p.1835A>T/p.D612V) of Lipin3 in a large family with hypertriglyceridemia (HTG) and obesity through whole-exome sequencing and Sanger sequencing. Functional studies revealed that the novel variant altered the half-life and stability of the Lipin3 protein. Hence, we generated Lipin3 heterozygous knockout (Lipin3-heKO) mice and cultured primary hepatocytes to explore the pathophysiological roles of Lipin3 in TG metabolism. We found that Lipin3-heKO mice exhibited obvious obesity, HTG, and non-alcoholic fatty liver disorder. Mechanistic study demonstrated that the haploinsufficiency of Lipin3 in primary hepatocytes may induce the overexpression and abnormal distribution of Lipin1 in cytosol and nucleoplasm. The increased expression of Lipin1 in cytosol may contribute to TG anabolism, and the decreased Lipin1 in nucleoplasm can reduce PGC1α, further leading to mitochondrial dysfunction and reduced TG catabolism. Our study suggested that Lipin3 was a novel disease-causing gene inducing obesity and HTG. We also established a relationship between Lipin3 and mitochondrial dysfunction.

关键词： Lipin3     Lipin1     hypertriglyceridemia     obesity     mitochondrial dysfunction    

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Non-genetic mechanisms of diabetic nephropathy

null

《医学前沿（英文）》 2017年 第11卷 第3期   页码 319-332 doi: 10.1007/s11684-017-0569-9

摘要：

Diabetic nephropathy (DN) is one of the most common microvascular complications in diabetes mellitus patients and is characterized by thickened glomerular basement membrane, increased extracellular matrix formation, and podocyte loss. These phenomena lead to proteinuria and altered glomerular filtration rate, that is, the rate initially increases but progressively decreases. DN has become the leading cause of end-stage renal disease. Its prevalence shows a rapid growth trend and causes heavy social and economic burden in many countries. However, this disease is multifactorial, and its mechanism is poorly understood due to the complex pathogenesis of DN. In this review, we highlight the new molecular insights about the pathogenesis of DN from the aspects of immune inflammation response, epithelial–mesenchymal transition, apoptosis and mitochondrial damage, epigenetics, and podocyte–endothelial communication. This work offers groundwork for understanding the initiation and progression of DN, as well as provides ideas for developing new prevention and treatment measures.

关键词： diabetic nephropathy     immune inflammatory response     epithelial–mesenchymal transition     apoptosis     mitochondrial damage     epigenetics     podocyte–endothelial communication    

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标题 作者 时间 类型 操作

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

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

Effects of resistin on insulin signaling in endothelial cells

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

期刊论文

New definition of metabolic dysfunction-associated fatty liver disease with elevated brachial-ankle pulse

期刊论文

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

Berberine alleviates myocardial diastolic dysfunction by modulating Drp1-mediated mitochondrial fission

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

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

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

期刊论文

Relationship of endothelial nitric oxide synthase gene polymorphism with blood pressure, lipid profile

TANG Zhongzhi, LI Junyao, YANG Jianhong

期刊论文

CD176 single-chain variable antibody fragment inhibits the adhesion of cancer cells to endothelial cells

null

期刊论文

Prognostic value of fasting glucose on the risk of heart failure and left ventricular systolic dysfunction

Hui Wang, Yang Zhang, Zhujun Shen, Ligang Fang, Zhenyu Liu, Shuyang Zhang

期刊论文

Clinical characteristics and risk factors of COVID-19 patients with chronic hepatitis B: a multi-center retrospective cohort study

期刊论文

Haploinsufficiency of Lipin3 leads to hypertriglyceridemia and obesity by disrupting the expression and nucleocytoplasmic localization of Lipin1

期刊论文

Non-genetic mechanisms of diabetic nephropathy

null

期刊论文