Natural human apoA-I mutations L141RPisa and L159RFIN alter HDL structure and functionality and promote atherosclerosis development in mice

•Transgenic mice expressing human apoA-I(L141R) or (L159R) have very low HDL levels.•HDL particles formed in these mice have preβ2 and α3, α4 electrophoretic mobility.•Anti-oxidant capacity of HDL containing apoA-I(L141R) or (L159R) is compromised.•Both apoA-I mutants are sufficient to promote diet-induced atherosclerosis in mice.