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Published on: December 9, 2022
Molecular Determinants of Chronic Venous Disease: A Comprehensive Review
Davide Costa1,2, Michele Andreucci3, Nicola Ielapi4
1Department of Law, Economics and Sociology, University "Magna Graecia" of Catanzaro, 88100 Catanzaro, Italy.
Insights
Chronic Venous Disease (CVD) involves complex genetic and cellular factors affecting leg veins. Understanding these molecular determinants, including extracellular matrix changes, is key to managing this common condition.
Area of Science:
- Vascular Biology and Medicine
Background:
- Chronic Venous Disease (CVD) is a prevalent condition affecting lower limb veins, leading to diverse symptoms and significant disability.
- Its complex etiology involves multifactorial genetic, proteomic, and cellular mechanisms impacting venous structure and function.
Purpose of the Study:
- To provide an up-to-date overview of the molecular determinants of Chronic Venous Disease.
- To explore the roles of genetic predisposition, hormonal influences, extracellular matrix imbalance, and endothelial dysfunction in CVD.
Main Methods:
- This review synthesizes current scientific literature on the molecular underpinnings of CVD.
- It focuses on genetic expressions, extracellular matrix alterations, and endothelial function.
Main Results:
- Genetic factors related to angiogenesis and vascular development influence CVD susceptibility.
- Alterations in the extracellular matrix (ECM) are identifiable and potentially targetable.
- Endothelial dysfunction plays a significant role in the pathophysiology of CVD.
Conclusions:
- Molecular determinants, including genetic and ECM factors, are crucial in understanding and potentially treating Chronic Venous Disease.
- Further research into these molecular pathways can lead to targeted therapeutic strategies for CVD.
Abstract:
Chronic Venous Disease (CVD) refers to several pathological and hemodynamic alterations of the veins of lower limbs causing a wide range of symptoms and signs with a high prevalence in the general population and with disabling consequences in the most severe forms. The etiology and pathophysiology of CVD is complex and multifactorial, involving genetic, proteomic, and cellular mechanisms that result in changes to the venous structure and functions. Expressions of several genes associated with angiogenesis, vascular development, and the regulation of veins are responsible for the susceptibility to CVD. Current evidence shows that several extracellular matrix alterations (ECM) could be identified and in some cases pharmacologically targeted. This review shows the most up to date information on molecular determinants of CVD in order to provide a complete overview of the current knowledge on this topic. In particular, the article explores the genetic influence, the hormonal influence, ECM imbalance, and histopathology of CVD and the role of endothelial dysfunction in CVD.
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