Platelet-Activating Factor Promotes the Development of Non-Alcoholic Fatty Liver Disease

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a multifaceted clinicopathological syndrome characterised by excessive hepatic lipid accumulation that causes steatosis, excluding alcoholic factors. Platelet-activating factor (PAF), a biologically active lipid transmitter, induces platelet activation upon binding to the PAF receptor. Recent studies have found that PAF is associated with gamma-glutamyl transferase, which is an indicator of liver disease. Moreover, PAF can stimulate hepatic lipid synthesis and cause hypertriglyceridaemia. Furthermore, the knockdown of the PAF receptor gene in the animal models of NAFLD helped reduce the inflammatory response, improve glucose homeostasis and delay the development of NAFLD. These findings suggest that PAF is associated with NAFLD development. According to reports, patients with NAFLD or animal models have marked platelet activation abnormalities, mainly manifested as enhanced platelet adhesion and aggregation and altered blood rheology. Pharmacological interventions were accompanied by remission of abnormal platelet activation and significant improvement in liver function and lipids in the animal model of NAFLD. These confirm that platelet activation may accompany a critical importance in NAFLD development and progression. However, how PAFs are involved in the NAFLD signalling pathway needs further investigation. In this paper, we review the relevant literature in recent years and discuss the role played by PAF in NAFLD development. It is important to elucidate the pathogenesis of NAFLD and to find effective interventions for treatment.

Differential expression of serum TM, PAF, and CD62P in patients with autologous arteriovenous fistula and the correlation with vascular access function

“…As a platelet activator, platelet‐activating factor (PAF) can induce platelet deformation, aggregation, and release, which is common in atherosclerosis research at present. 14 Correa Costa and other scholars have found through animal experiments that PAF or PAF‐like molecules can enhance renal dysfunction and fibrosis and may promote epithelial to mesenchymal transition. 15 However, there are few reports on the relationship between the expression of TM, PAF, and CD62P in serum of AVF patients and vascular access function.…”

“…Scholars such as Yu have found 13 that CD62P is associated with the efficacy of hemodialysis in the treatment of end‐stage kidney disease, and can also be used to predict efficacy. As a platelet activator, platelet‐activating factor (PAF) can induce platelet deformation, aggregation, and release, which is common in atherosclerosis research at present 14 . Correa Costa and other scholars have found through animal experiments that PAF or PAF‐like molecules can enhance renal dysfunction and fibrosis and may promote epithelial to mesenchymal transition 15 .…”

Associations between healthy food groups and platelet-activating factor, lipoprotein-associated phospholipase A2 and C-reactive protein: a cross-sectional study

“…PAF has been shown to be associated with many CVDs including coronary heart disease, acute myocardial infarction, heart failure and stroke [ 20 – 23 ]. PAF is further involved in other metabolic chronic diseases such as diabetes and non-alcoholic fatty liver disease [ 24 – 26 ].…”

Interrelationships among platelet‐activating factor and lipoprotein‐associated phospholipase A2 activity and traditional cardiovascular risk factors

“…PAF increases reactive oxygen species leading to LDL oxidation, increases endothelial permeability and stimulates the differentiation of monocytes into macrophages 17–21 . PAF is associated with numerous CVDs such as, heart failure, acute myocardial infarction, coronary heart disease (CHD), and stroke 22–25 and other related inflammatory chronic diseases such as diabetes and nonalcoholic fatty liver disease where PAF stimulates hepatic lipid synthesis and causes hypertriglyceridemia 26–28 …”

“…[17][18][19][20][21] PAF is associated with numerous CVDs such as, heart failure, acute myocardial infarction, coronary heart disease (CHD), and stroke [22][23][24][25] and other related inflammatory chronic diseases such as diabetes and nonalcoholic fatty liver disease where PAF stimulates hepatic lipid synthesis and causes hypertriglyceridemia. [26][27][28] Lp-PLA 2 is a 50-kD, Ca 2+ independent phospholipase (EC 3.1. 1.47) which belongs to Group VII of the superfamily of PLA2 enzymes.…”