REVIEWDyslipidemia and inflammation: an evolutionary conserved mechanism
Section snippets
Changes in HDL lipoprotein during inflammation
It is well known that HDL particles are fundamental for cholesterol reverse transport, and protect from coronary disease development.21 There are several mechanisms through which inflammation and cytokines can modify the size, composition and function of HDLs. During APR a wide range of changes in HDL apolipoprotein and enzymes occurs. These changes in HDL particles caused by inflammation not only reduce HDL-C levels but they also alter anti-oxidant properties of HDL and LDL protection from
Changes in VLDL lipoprotein and TGs during inflammation
Elevation of TG levels is considered as an independent cardiovascular risk factor, especially in the diabetic population.112, 113, 114 Nevertheless, it is difficult to establish an independent association between TGs and cardiovascular risk due to their close relation with HDL-C levels.115
Changes in LDL lipoprotein and cholesterol during inflammation
Most of the LDL particles are derived from the intravascular catabolism of VLDL. Catabolism of LDL occurs in both peripheral cells and the liver and is facilitated by both LDL-receptor- (LDL-R-) mediated and non-receptor-mediated pathways. Clinical and epidemiological studies have shown LDL-C as one of the most important cardiovascular risk factors.
Lipoprotein(a), inflammation and tissue repair
It has been hypothesized that Lp(a) could offered an evolutionary advantage to humans by promoting or accelerating the healing of wounds and the repair of tissue injuries and vascular lesions.199 In fact, Lp(a) behaves as an acute-phase reactant. The sequence of the apo(a) gene contains several IL-6-responsive elements that enhance transcription of the gene.200 IL-6 generates a marked, dose-dependent enhancement of apo(a) mRNA synthesis that leads to the accumulation of Lp(a) particles in
Conclusions
Lipoproteins can decrease the toxicity of a variety of harmful biological and chemical agents. Lipoproteins are directly involved in the host response to infection and tissue destruction. During acute illness, delivery of cholesterol to the liver for excretion is altered to allow cholesterol to remain in the tissues where it is needed for repair and regeneration of damaged membranes. In fact, lipoproteins have been found to be potent inhibitors of the infectivity of different viruses and to
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