Soluble endoglin, hypercholesterolemia and endothelial dysfunction

Rathouska, Jana; Ježková, Kateřina; Němečková, Ivana; Nachtigal, Petr

doi:10.1016/j.atherosclerosis.2015.10.003

Cited by 53 publications

(61 citation statements)

References 52 publications

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“…Although sEng inhibits TGF-β function, leading to enhanced atherogenesis, 3 sEng levels in patients with atherosclerotic diseases or risk factors have not been clarified.…”

Section: Discussionmentioning

confidence: 99%

“…3 Inhibition of endoglin enhances TGF-β1 signaling to suppress the migration and growth of endothelial cells, thus suggesting its inhibitory effect on TGF-β1. 4 Endoglin is highly expressed in endothelial cells of inflamed tissues, healing wounds, vascular injury, and angiogenesis.…”

Section: See Accompanying Editorial On Page 10mentioning

confidence: 99%

“…10 Endoglin is released into circulation as a soluble form (soluble endoglin [sEng]) in various conditions related to endothelial injury and inflammation. 3 Role of sEng in regulating TGF-β signaling is considered as a TGF-β antagonist. 3 Increased sEng levels in blood and enhanced atherosclerosis with decreased endoglin expression were demonstrated in apolipoprotein E/low-density lipoprotein (LDL) receptor knockout mice fed by cholesterol-rich diet.…”

Section: See Accompanying Editorial On Page 10mentioning

confidence: 99%

“…3 Role of sEng in regulating TGF-β signaling is considered as a TGF-β antagonist. 3 Increased sEng levels in blood and enhanced atherosclerosis with decreased endoglin expression were demonstrated in apolipoprotein E/low-density lipoprotein (LDL) receptor knockout mice fed by cholesterol-rich diet. 11 Increased sEng levels may result in reduced TGF-β signaling, leading to enhanced atherosclerosis.…”

Section: See Accompanying Editorial On Page 10mentioning

confidence: 99%

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Plasma Soluble Endoglin Levels Are Inversely Associated With the Severity of Coronary Atherosclerosis—Brief Report

Saita

Miura

Suzuki-Sugihara

et al. 2017

ATVB

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Objective-Transforming growth factor-β inhibits migration and proliferation of endothelial and smooth muscle cells.Endoglin is a transmembrane receptor for transforming growth factor-β1 and transforming growth factor-β3. Endoglin is released into blood as a soluble form (soluble endoglin [sEng]), but plasma sEng levels in patients with coronary artery disease (CAD) have not been elucidated. Approach and Results-We measured plasma sEng levels in 244 patients undergoing coronary angiography. The severity of coronary atherosclerosis was evaluated as the numbers of >50% stenotic vessels and segments. CAD was found in 147 patients, of whom 55 had 1-vessel, 42 had 2-vessel, and 50 had 3-vessel disease. Compared with 97 patients without CAD, 147 with CAD had lower sEng levels (median 4.04 versus 4.37 ng/mL; P<0.005). A stepwise decrease in sEng levels was found based on the number of stenotic vessels: 4.37 in CAD(−), 4.23 in 1-vessel, 4.13 in 2-vessel, and 3.74 ng/mL in 3-vessel disease (P<0.005). sEng levels inversely correlated with the number of stenotic segments (r=−0.25; P<0.001). In multivariate analysis, sEng was an independent factor for 3-vessel disease and CAD. Odds ratios for CAD and 3-vessel disease were 0.97 (95% confidence interval, 0.95-0.99; P<0.02) and 0.96 (95% confidence interval, 0.93-0.99; P<0.01) for a 0.1 ng/mL increase in sEng levels, respectively. Conclusions-Plasma sEng levels were low in patients with CAD, especially 3-vessel disease, and were inversely associated with the severity of coronary atherosclerosis. The study sponsors had no role in the design, analysis, and interpretation of the study. The online-only Data Supplement is available with this article at http://atvb.ahajournals.org/lookup/suppl

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“…Although sEng inhibits TGF-β function, leading to enhanced atherogenesis, 3 sEng levels in patients with atherosclerotic diseases or risk factors have not been clarified.…”

Section: Discussionmentioning

confidence: 99%

Section: See Accompanying Editorial On Page 10mentioning

confidence: 99%

Section: See Accompanying Editorial On Page 10mentioning

confidence: 99%

Section: See Accompanying Editorial On Page 10mentioning

confidence: 99%

See 2 more Smart Citations

Plasma Soluble Endoglin Levels Are Inversely Associated With the Severity of Coronary Atherosclerosis—Brief Report

Saita

Miura

Suzuki-Sugihara

et al. 2017

ATVB

View full text Add to dashboard Cite

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“…The imbalance of angiogenesis and anti‐angiogenic factors in the maternal circulation plays a key role in the pathogenesis of preeclampsia. Soluble endoglin (sEng) is an anti‐angiogenic factor, a soluble structure of the extracellular domain structure of Eng, with a molecular weight of 65 k Da . sEng is also a cell surface co‐receptor of TGF‐β, which is competitive.…”

Section: Introductionmentioning

confidence: 99%

The diagnosis values of serum STAT4 and sEng in preeclampsia

Zhang¹,

Li²,

Zhou³

et al. 2019

Clinical Laboratory Analysis

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Objective To detect the levels of signal transducer and activator of transcription 4 (STAT4) and soluble endoglin (sEng) in preeclampsia patients and analyze the diagnostic values of STAT4 and sEng in preeclampsia. Methods Fifty‐four pregnant women with preeclampsia from October 2017 to June 2018 were included in this study. Twenty‐eight matched healthy pregnant women were set as the control group. The general clinical characteristics were measured. Serum STAT4 and sEng were detected by ELISA. Correlation between STAT4 and sEng, and their diagnostic value in preeclampsia were analyzed. Results Compared with control, the prothrombin time in preeclampsia was significantly lower, while the mean arterial pressure, 24‐hour urine protein, serum creatinine, fibrinogen, and ALT were significantly higher. The circulating levels of STAT4 and sEng were significantly increased in the preeclampsia. The serum levels of STAT4 and sEng in preeclampsia were positively correlated. For the diagnosis of preeclampsia by the serum STAT4, AUC is 0.902, and the sensitivity and specificity are 0.893 and 0.929. By the serum sEng, AUC is 0.873, and the sensitivity and specificity are 0.816 and 0.905. Conclusion The serum levels of STAT4 and sEng were significantly increased in preeclampsia with disease severity status, which have promise as diagnostic markers in preeclampsia.

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Whole-Body Distribution and Clinical Association of Telangiectases in Systemic Sclerosis

et al. 2018

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IMPORTANCE In systemic sclerosis (SSc), to date, no study has precisely described the total number and fine distribution of telangiectases (TAs), their clinical association with the disease, and the biological mechanisms causing their development. OBJECTIVES To describe the whole-body distribution of TAs and assess the association between the whole-body TA number and the characteristics of patients with SSc. DESIGN, SETTING, AND PARTICIPANTS A single-center, cross-sectional study was conducted between July 11, 2016, and March 15, 2017, at the National Referral Centre for Rare Systemic and Autoimmune Diseases in France. A population-based sample of 106 adults who fulfilled the 2013 American College of Rheumatology/European League Against Rheumatism criteria for SSc were included; 8 patients who had previously received laser treatment for TAs were excluded. MAIN OUTCOMES AND MEASURES The number of TAs on the whole body (total and those >5 mm) and TA distribution in different areas were recorded. The association with clinical and biological data was studied using univariate and multivariate linear regression. RESULTS A total of 106 patients (83 [78.3%] women) were enrolled, including 12 with precapillary pulmonary hypertension (PH). Mean (SD) age was 60.6 (13.5) years. Telangiectasia distribution was 37.2% on the face, 33.2% on the upper limbs, including 26.4% on the hands, 28.1% on the trunk, including 17.1% for the upper part of the trunk, and 1.5% on the lower limbs. In analysis using the multivariate linear regression model, the whole-body TA number was independently associated with male sex (percentage change, 144.4%; 95% CI, 7.5% to 455.9%; P = .03), PH (162.8%; 95% CI, 5.6% to 553.8%; P = .04), history of pulmonary embolism (336.4%; 95% CI, 39.0% to 1270.1%; P = .01), glomerular filtration rate (−1.6%; 95% CI, −3.2% to −0.1% per 1-mL/min/1.73 m 2 increase; P = .04), and soluble endoglin level (28.2%; 95% CI, 1.2% to 62.5% per 1-ng/mL increase; P = .04). Receiver operating characteristic analyses assessing the ability of TAs to identify the presence of PH revealed that the area under the curve was significant for the TA number on the whole body (0.77; 95% CI, 0.57 to 0.88), on the hands and face (0.81; 95% CI, 0.57 to 0.91), and on the hands (95% CI, 0.77; 95% CI, 0.57 to 0.89). CONCLUSIONS AND RELEVANCE In the patients in this study with SSc, TAs were predominantly located on the face, hands, and the upper part of the trunk. Telangiectases appeared to be associated with vasculopathy features of SSc, particularly with PH and soluble endoglin levels.

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Soluble endoglin, hypercholesterolemia and endothelial dysfunction

Cited by 53 publications

References 52 publications

Plasma Soluble Endoglin Levels Are Inversely Associated With the Severity of Coronary Atherosclerosis—Brief Report

Plasma Soluble Endoglin Levels Are Inversely Associated With the Severity of Coronary Atherosclerosis—Brief Report

The diagnosis values of serum STAT4 and sEng in preeclampsia

Whole-Body Distribution and Clinical Association of Telangiectases in Systemic Sclerosis

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