“…It has been proposed that LPL protein lacking any lipase activity may function as a bridge between apoB-containing lipoproteins and proteoglycans on vessel walls, thereby retaining atherogenic lipoproteins on endothelial cells, and leading to the progression of atherosclerosis (7,14). In fact, patients with complete LPL deficiency, whereby both enzymatic activity and protein mass are absent, reportedly exhibit a nonatherogenic phenotype (15,16), while patients with missense mutations which result in the absence of LPL activity with retention of the LPL protein are prone to atherogenesis (4,(6)(7)(8). Therefore, functionally inactive R243H-LPL protein may have played a role in the development of the severe atherosclerosis observed in this patient.…”