APOB and familial hyperaldosteronism: From our results in FH patients, we could not exclude that the higher content of C3 in the atherosclerotic ECM results from the LDL flux into the intimal arterial wall and the retention of ApoB-rich lipoprotein particles in the intimal ECM space by binding to proteoglycans, which in turn favors their modification to form aggregates (agLDL) [40,41].