Lipoproteins and the apolipoproteins (apo) that they carry are major determinants of cardiovascular diseases (CVD) as well as metabolic, renal and inflammatory chronic disorders either directly or through mediation of risk factors. The notion that elevated low-density lipoprotein cholesterol (LDL-C) and apoB levels are related to the acquisition of CVD and, high-density lipoprotein cholesterol (HDL-C) and apoA-I indicate protection against CVD has been challenged in the past decade. Advanced age, adiposity, ethnicity or impaired glucose intolerance rendered autoimmune activation in an environment of pro-inflammatory state/oxidative stress and may disrupt the linear risk association between lipoproteins. Areas covered: This review summarizes the modified risk associations of lipoproteins and apolipoprotein by an environment of chronic systemic low-grade inflammation with special emphasis on the non-linear relationship of lipoprotein(a) [Lp(a)], a biomarker of renewed interest in cardiometabolic risk. Expert commentary: It seems that autoimmune activation in an environment of pro-inflammatory state/oxidative stress not only disrupts the linear risk association between lipoproteins, but also may cause interference in immunoassays. Hence, methodological improvement in immunoassays and much further research focusing on population segments susceptible to a pro-inflammatory state is necessary for further advances in knowledge.
Keywords: Apolipoproteins; chronic kidney disease; coronary heart disease; lipoproteins; mortality; oxidized phospholipids.