Abstract
CD36 (also known as platelet glycoprotein IV) is expressed by a variety of different
cell entities, where it possesses functions as a signaling receptor, but additionally
acts as a transporter for long-chain fatty acids. This dual function of CD36 has been
investigated for its relevance in immune and nonimmune cells. Although CD36 was first
identified on platelets, the understanding of the role of CD36 in platelet biology
remained scarce for decades. In the past few years, several discoveries have shed
a new light on the CD36 signaling activity in platelets. Notably, CD36 has been recognized
as a sensor for oxidized low-density lipoproteins in the circulation that mitigates
the threshold for platelet activation under conditions of dyslipidemia. Thus, platelet
CD36 transduces atherogenic lipid stress into an increased risk for thrombosis, myocardial
infarction, and stroke. The underlying pathways that are affected by CD36 are the
inhibition of cyclic nucleotide signaling pathways and simultaneously the induction
of activatory signaling events. Furthermore, thrombospondin-1 secreted by activated
platelets binds to CD36 and furthers paracrine platelet activation. CD36 also serves
as a binding hub for different coagulation factors and, thus, contributes to the plasmatic
coagulation cascade. This review provides a comprehensive overview of the recent findings
on platelet CD36 and presents CD36 as a relevant target for the prevention of thrombotic
events for dyslipidemic individuals with an elevated risk for thrombosis.
Keywords
platelets - CD36 - Erk5 - signaling - cAMP - cGMP - thrombospondin - fibrin - coagulation
