LDLR and atherosclerosis: However, on an atherosclerosis-prone Apobec-1 and LDL receptor double-knockout murine model, Egan and colleagues [23] have shown that unlike indomethacin, urinary excretion of only PGI-M (but not other major metabolites of TXA2, TXB2, or prostacyclin) was reduced by COX-2 inhibition.