Figure 3.

Platelets in non-alcoholic fatty liver disease (NAFLD). Obesity and insulin resistance promote the development of NAFL, which leads to a pro-coagulant state (e.g., increased von Willebrand factor [vWF] and plasminogen activator inhibitor [PAI-1]) and hyperaggregable platelets (e.g., elevated GPVI signaling, aldolase activity, platelet priming and aspirin resistance). The interaction with leukocytes and the release of granule content by activated platelets either promote (CD40 ligand [CD40L], chemokine (C-X-C motif) ligand [CXCL4] and serotonin [5-HT], thromboxane A2 [TxA2]) or prevent (thrombospondin-1 [TSP-1]) NAFLD progression.