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Autophagy and Venous Endothelial Function

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關鍵詞

抽象

The molecular mechanisms involved in venous endothelial dysfunction are largely unknowns. Autophagy is an intracellular mechanism devoted to the removal of damaged cytoplasmic elements. Previous evidence demonstrated that activation of autophagy exerts beneficial effects in the cardiovascular system, reducing cardiac damage and improving cardiac function in response to stress. However, the association between venous endothelial dysfunction and autophagy remains to be characterized. In this study the investigators will test whether reactivation of autophagy through a natural compound (spermidine) is able to improve vascular function in saphenous veins derived from patients subjected to saphenectomy. The same outcome will be evaluated in saphenous veins isolated from patients with atherosclerotic obstructive disease of the lower limbs subjected revascularization through implantation of venous by-pass.

描述

Endothelial dysfunction contributes to different cardiovascular diseases, such as atherosclerosis, myocardial infarction, stroke and peripheral artery diseases. Recent evidence also demonstrated that endothelial dysfunction is associated with vascular venous diseases. In this regard, venous endothelial dysfunction contributes to the development of varicose veins and deep vein thrombosis. Disequilibrium in endothelial function is also present in venous traits derived from saphenous veins which are routinely used as aortocoronary by-pass. The molecular mechanisms involved in venous diseases require further investigations. Autophagy, the intracellular mechanism devoted to the removal of dysfunctional or senescent cytoplasmic elements may represent a new therapeutic target for the treatment of vascular diseases. In this regard, it has been demonstrated that the enhancement of autophagy limits cardiac injury in pre-clinical models of cardiovascular diseases. However, the association between autophagy and vascular disease is still unknown in humans. Spermidine is a natural activator of autophagy which has been demonstrated to extend lifespan in mice and to reduce cardiac dysfunction through autophagy-dependent mechanisms. The objectives of this study will be the following: 1) to test whether spermidine is able to improve vascular function and to reduce oxidative stress in saphenous veins obtained from patients subjected to saphenectomy due to chronic venous insufficiency or varicose veins; 2) to test whether spermidine is able to improve vascular function in saphenous veins derived from patients with atherosclerotic obstructive disease of lower limbs subjected to revascularization through implantation of arteriosus by-pass. In a different set of experiments, the investigators will also test whether vein portions incubated with spermidine show increased autophagy and decreased markers of oxidative stress with respect to controls. The investigators expect that venous segments treated with spermidine will show an amelioration of endothelial function

日期

最後驗證: 09/30/2019
首次提交: 10/21/2019
提交的預估入學人數: 10/21/2019
首次發布: 10/23/2019
上次提交的更新: 10/23/2019
最近更新發布: 10/27/2019
實際學習開始日期: 11/30/2019
預計主要完成日期: 02/29/2020
預計完成日期: 05/31/2020

狀況或疾病

Venous Disease

-

手臂組

干預/治療
Group 1
Patients subjected to saphenectomy due to chronic venous insufficiency or varicose veins
Group 2
Patients with atherosclerotic obstructive disease of lower limbs

資格標準

有資格學習的年齡 18 Years 至 18 Years
有資格學習的性別All
取樣方式Probability Sample
接受健康志願者沒有
標準

Inclusion Criteria:

- Eligible subjects undergoing saphenectomy

- Patients with chronic venous insufficiency

- Patients with varicose veins

- Eligible subjects undergoing peripheral artery revascularization through implantation of venous by-pass derived from saphenous vein

- Acceptance and signature of the informed consent

Exclusion Criteria:

- Chronic and acute Inflammatory diseases

- Immunological and rheumatic diseases

- Pre-existing or ongoing neoplasms

- Infectious diseases

- Previous organ transplantation

- Treatment with pharmacological therapies able to modulate autophagy, i. e. rapamycin and derivative compounds (rapalogues).

- Antioxidant therapies in the last three months

- Patients with surgical technical complications

結果

主要結果指標

1. Evaluation of endothelial function in venous samples from patients with venous insufficiency before and after treatment with autophagy enhancer spermidine [Immediately after the sampling]

Ex vivo vascular reactivity experiments performed on isolated veins treated or not with spermidine ex vivo.

次要成果指標

1. Impact of autophagy on endothelial venous function [6 months]

Quantification by immunoblot of markers of autophagy (LC3, p62, Beclin1, Atg5, Atg7, Ulk1) and its statistical correlation with venous endothelial function

2. Correlation between autophagy, oxidative stress and endothelial function [6 months]

Quantification by immunoblot of markers of autophagy and oxidative stress and statistical correlation with venous endothelial function

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