**6. Conclusions**

Age-related changes in morphology and function of LSECs apparently contribute to dyslipidemia and, as a consequence, to the development of cardiovascular disease. Old age is associated with reduced fenestrae in the LSEC which impedes the hepatic uptake of chylomicron remnants and possibly other lipoproteins. In addition, aging is associated with reduced LSEC endocytic capacity which will impact on circulating levels of oxLDL. Thus the LSEC is a novel therapeutic target for the treatment of age-related dyslipidemia and has great potential for the prevention of atherosclerosis and cardiovascular events.
