Adipokines in Hepatic Angiogenesis

Review Article

Austin Biomark Diagn. 2015;2(1): 1016.

Adipokines in Hepatic Angiogenesis

Michal Kukla*, Marek Waluga and Edward Surma

Department of Gastroenterology and Hepatology, Medical University of Silesia, Poland

*Corresponding author: Michal Kukla, Department of Gastroenterology and Hepatology, Medical University of Silesia, ul. Medykow 14, 40-752 Katowice, Poland,

Received: December 15, 2014; Accepted: March 16, 2015; Published: March 24, 2015

Abstract

Hepatic angiogenesis in the course of chronic hepatitis merely represents a homeostatic mechanism directed to ensuring a necessary oxygen supply or one that plays an additional pathogenic role contributing to liver damage. Additionally, in chronic hepatitis, there is a switch toward proangiogenic factors. Many efforts have been directed to explain the mechanisms involved in angiogenesis during the progression of liver fibrosis. Recent data indicate that hepatic angiogenesis and fibrosis are closely related in both clinical and experimental conditions. Adipokines not only regulate adipose tissue and glucose metabolism, but also influence inflammation, fibrogenesis and production of proangiogenic agents. This short review briefly described a possible role of some adipokines in hepatic neovessels formation during liver morbidity.

Keywords: Adipokines; Angiogenesis; Chronic hepatitis; Liver; Fibrosis; Visfatin

Introduction

Angiogenesis, the formation of new vascular structures from preexisting vessels, occurs in Chronic Liver Diseases (CLDs) [1,2]. Hepatic angiogenesis in the course of chronic hepatitis merely represents a homeostatic mechanism directed to ensuring a necessary oxygen supply or one that plays an additional pathogenic role contributing to liver damage [3,4].

Angiogenesis in CLDs can result from two pathogenic pathways (Figure 1). Firstly, neo-angiogenesis is evoked and potentiated in hepatic tissue by progressive tissue hypoxia. Accumulation of inflammatory cells and development of fibrosis may enhance resistance of liver tissue to blood flow and oxygen supply, resulting into hypoxia [5]. On the other hand accumulated evidences indicate hypoxia alone could be important in the stimulation of angiogenesis and can also stimulate inflammation leading to a viscous circle between inflammation and angiogenesis [6-8]. Hypoxia activates angiogenesis as a result of signaling mediated by Hypoxia-Inducible Factors (HIFs) [7-10]. Also hepatic steatosis enhances disturbances in hepatocyte energy regulation provoking hypoxia and cell injury with subsequent development of neoangiogenesis [11,12]. These circumstances contribute to an up-regulation of proangiogenic factors leading to vascular remodeling and neovessels formation [13]. Secondly, the process of liver chronic wound healing is a hallmark for fibrogenic CLDs. It is associated with an increased expression of growth factors, cytokines and Metalloproteinases (MMPs) with an underlying proangiogenic activity [14]. Angiogenesis in liver is characterized by capillarization of the sinusoids [15]. Structures responsible for proliferation and maturation of new blood vessels in the liver are Hepatic Stellate Cells (HSCs), Kupffer cells, regenerating hepatocytes and existing Endothelial Cells (ECs) [3].