High‐density lipoprotein 3 and apolipoprotein <scp>A</scp>‐<scp>I</scp> alleviate platelet storage lesion and release of platelet extracellular vesicles

Abstract

nHDL3 and apoA-I improve PLT membrane homeostasis and intracellular lipid processing and increase CE efflux, antagonizing PSL-related reduction in PLT viability and function and PL-EV release. We suggest uptake and catabolism of nHDL3 into the PLT open canalicular system. As supplement in PLCs, nHDL3 or apoA-I from Fraction IV of plasma ethanol fractionation have the potential to improve PLC quality to prolong storage.