关键词: JNK ageing chronic venous insufficiency osteogenesis venous reflux

Mesh : Adult Aged Aging / physiology Blood Circulation / physiology Calcinosis / pathology physiopathology surgery Chronic Disease Cross-Sectional Studies Female Humans JNK Mitogen-Activated Protein Kinases / analysis metabolism MAP Kinase Signaling System / physiology Male Middle Aged Saphenous Vein / pathology surgery Venous Insufficiency / pathology physiopathology surgery

来  源:   DOI:10.7150/ijms.54052   PDF(Pubmed)

Abstract:
Chronic venous insufficiency (CVI) is one of the most common vascular pathologies worldwide. One of the risk factors for the development of CVI is aging, which is why it is related to senile changes. The main trigger of the changes that occur in the venous walls in CVI is blood flow reflux, which produces increased hydrostatic pressure, leading to valve incompetence. The cellular response is one of the fundamental processes in vascular diseases, causing the activation of cell signalling pathways such as c-Jun N-terminal kinase (JNK). Metabolic changes and calcifications occur in vascular pathology as a result of pathophysiological processes. The aim of this study was to determine the expression of JNK in venous disease and its relationship with the role played by the molecules involved in the osteogenic processes in venous tissue calcification. This was a cross-sectional study that analyzed the greater saphenous vein wall in 110 patients with (R) and without venous reflux (NR), classified according to age. Histopathological techniques were used and protein expression was analysed using immunohistochemistry techniques for JNK and markers of osteogenesis (RUNX2, osteocalcin (OCN), osteopontin (OPN)). Significantly increased JNK, RUNX2, OCN, OPN and pigment epithelium-derived factor (PEDF) protein expression and the presence of osseous metaplasia and amorphous calcification were observed in younger patients (<50 years) with venous reflux. This study shows for the first time the existence of an osteogenesis process related to the expression of JNK in the venous wall.
摘要:
慢性静脉功能不全(CVI)是世界范围内最常见的血管病变之一。CVI发展的危险因素之一是衰老,这就是为什么它与老年变化有关。CVI中静脉壁变化的主要触发因素是血流回流,产生增加的静水压力,导致阀门不称职。细胞反应是血管疾病的基本过程之一,引起细胞信号传导途径的激活,如c-JunN末端激酶(JNK)。由于病理生理过程,在血管病理学中发生代谢变化和钙化。这项研究的目的是确定JNK在静脉疾病中的表达及其与参与成骨过程的分子在静脉组织钙化中所起的作用的关系。这是一项横断面研究,分析了110例(R)和无静脉回流(NR)患者的大隐静脉壁,按年龄分类。使用组织病理学技术,并使用免疫组织化学技术分析JNK和成骨标志物(RUNX2,骨钙蛋白(OCN),骨桥蛋白(OPN)。JNK显著增加,RUNX2,OCN,在静脉回流的年轻患者(<50岁)中观察到OPN和色素上皮衍生因子(PEDF)蛋白表达以及骨化生和无定形钙化的存在。这项研究首次显示了与JNK在静脉壁中的表达有关的成骨过程的存在。
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