Dear Colleagues,

More than 50 years have passed since the term PAF (Platelet-Activating Factor) was first coined by Benveniste, Henson, and Cochrane in 1972 to describe the activities of PAF that were known until then, namely platelet activation and aggregation. Its chemical structure was elucidated in 1979 as a glyceryl-ether lipid (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) by Demopoulos, Pinckard, and Hanahan. PAF is now recognized as a primitive lipid mediator with several actions in almost all human systems, and has been implicated in various physiological and pathophysiological processes.

PAF is a potent inflammatory mediator that is implicated in a variety of conditions and chronic diseases, such as allergies, asthma, infections, cancer, renal diseases, cerebrovascular and central nervous system disorders, cardiovascular diseases and recently in COVID-19. In addition to its role in acute inflammation, PAF is also involved in cell signaling mechanisms for a number of physiological processes, including apoptosis, wound healing, reproduction and angiogenesis.

PAF exerts its actions mainly by binding to the its G-protein-coupled receptor (PAF-R) located on the plasma and nuclear membrane and expressed by a variety of cells and tissues. PAF-R also interacts with PAF-like oxidized phospholipids (Ox-PLs) and recognizes components of the bacterial wall, such as lipoteichoic acid and lipopolysaccharides. PAF action and metabolism can be modulated in different ways, such as by diet, lifestyle, and environmental factors. PAF has been a therapeutic target for many chronic diseases, and therefore, several natural and synthetic origin PAF antagonists have been studied across several disciplines.

This Special Issue aims to integrate current knowledge regarding the functions of PAF in an attempt to determine novel therapeutics that most likely target PAF in conjunction with various other inflammatory mediators.

Prof. Smaragdi Antonopoulou
Guest Editor