Vascular pathobiology in chronic liver disease and cirrhosis - current status and future directions.
Vascular pathobiology in chronic liver disease and cirrhosis - current status and future directions.
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DOI：
10.1016/j.jhep.2014.05.047
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发表时间：
2014-10
影响因子：
25.7
通讯作者：
Rockey DC
中科院分区：
文献类型：
--
作者：
Iwakiri Y;Shah V;Rockey DC
慢性肝病与肝内外血管的显著改变有关。由于这些变化，肝血管和门静脉高压症领域最近已经紧密地整合到更广泛的血管生物学学科中。随着血管生物学的发展，对血管过程的深入了解有助于更好地理解与门静脉高压症和慢性肝病相关的动态血管变化的机制。在这种背景下，肝血管细胞，如肝窦内皮细胞和周细胞样肝星状细胞，相互之间具有旁分泌和自分泌作用，相互之间具有密切的联系。这些细胞在肝纤维化/肝硬变和门脉高压的发病机制中起重要作用。此外，最近还发现了多种信号通路。这些途径包括涉及细胞因子的生长因子途径，如转化生长因子β、血小板衍生生长因子等，以及各种血管活性多肽和其他分子。肝损伤的一个早期和持续的特征是肝内阻力的增加；这与导致门脉高压的肝血管细胞及其信号通路的变化有关。一个重要的概念是，这一过程将信号聚集到肝外循环，导致该系统的细胞和信号通路紊乱，最终导致内脏和体循环中侧支血管的形成和动脉血管扩张，这凭借欧姆定律(压力=阻力×流量)的水力推导，加剧了门静脉高压。本文对门脉高压的基础生物学的研究现状和未来发展方向进行了详细的综述，重点介绍了肝内细胞的生理学、病理生理学和信号转导，以及肠系膜血管循环中的细胞。文章还强调了近期研究的翻译意义和未来的发展方向。
Chronic liver disease is associated with remarkable alterations in the intra- and extrahepatic vasculature. Because of these changes, the fields of liver vasculature and portal hypertension have recently become closely integrated within the broader vascular biology discipline. As developments in vascular biology have evolved, a deeper understanding of vascular processes has led to a better understanding of the mechanisms of the dynamic vascular changes associated with portal hypertension and chronic liver disease. In this context, hepatic vascular cells, such as sinusoidal endothelial cells and pericyte-like hepatic stellate cells, are closely associated with one another, where they have paracrine and autocrine effects on each other and themselves. These cells play important roles in the pathogenesis of liver fibrosis/cirrhosis and portal hypertension. Further, a variety of signaling pathways have recently come to light. These include growth factor pathways involving cytokines such as transforming growth factor β, platelet derived growth factor, and others as well as a variety of vasoactive peptides and other molecules. An early and consistent feature of liver injury is the development of an increase in intra-hepatic resistance; this is associated with changes in hepatic vascular cells and their signaling pathway that cause portal hypertension. A critical concept is that this process aggregates signals to the extrahepatic circulation, causing derangement in this system’s cells and signaling pathways, which ultimately leads to the collateral vessel formation and arterial vasodilation in the splanchnic and systemic circulation, which by virtue of the hydraulic derivation of Ohm’s law (pressure = resistance × flow), worsens portal hypertension. This review provides a detailed review of the current status and future direction of the basic biology of portal hypertension with a focus on the physiology, pathophysiology, and signaling of cells within the liver, as well as those in the mesenteric vascular circulation. Translational implications of recent research and the future directions that it points to are also highlighted.
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影响因子：
2.1
作者：
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通讯作者：
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影响因子：
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作者：
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DOI：
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影响因子：
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作者：
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作者：
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