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Aim and scope: This review is intended to update the knowledge, but above all, to understand the difference between "normal" level vs. biological level of LDL cholesterol (LDL-C) and the physiology of the metabolism of lipoproteins with apoprotein B100 (LP-apoB100). Such medical knowledge is fundamental before introducing to the world of dyslipidemia, atherosclerosis, and pharmacotherapeutics.

Unfortunately, the teaching of the enunciated concepts -as a starting point for basic knowledge- is frequently mixed with multiple related topics, among them: the pathophysiology analysis of LP-apoB100 metabolism, that is, of dyslipidemias; the description of transgenic animal models for their study; Mendelian randomization studies of the correlation between certain genetic patterns or single nucleotide polymorphism with specific dyslipidemias and atherosclerotic cardiovascular disease (ASCVD), the study at different levels of atherosclerosis -main consequence of the abnormal metabolism of LP-apoB100- and finally, the treatment of atherogenic dyslipidemias, atherosclerosis, and ASCVD.

Hence, teaching these concepts is complex, and therefore, also the learning by the non-specialist physician of these priority chapters in modern medicine. This review is premised on the following sentence: “LP-apoB100 were not created by nature to cause atherosclerosis”.

In this contemporary review we will analyze current knowledge on: the physiological value of LP-apoB100 with an emphasis on LDL, metabolism of LP-apoB100 (assembly and secretion of VLDL by the hepatocyte, circulatory transformation of VLDL to IDL, circulatory/hepatic transformation of IDL to LDL and hepatobiliary elimination of LDL) and finally LDL oxidation and elimination by reverse transport.

As Goldstein and Brown anticipated in the 1970s: "only by understanding the metabolism of LP-apoB100 will we be able to develop drugs to treat hypercholesterolemia and reduce its implicit atherosclerotic cardiovascular risk."