Figure 1.

Oxidation, inflammation, and disturbances in energy metabolism are closely related. To date, the evidence reported suggests that excessive production of reactive oxygen species (ROS) would inhibit paraoxonase-1 (PON1) activity in high-density lipoprotein (HDL) particles and in the mitochondrial membranes of somatic cells. At the same time, it would stimulate the synthesis of chemokine (C-C motif) ligand 2 (CCL2) through several pathways, notably that of pathogen-associated molecular patterns/damage-associated molecular patterns/pattern-recognition receptors (PAMP/DAMP/PRR). The decrease in PON1 activity and the increase in CCl2 would cause alterations in mitochondrial metabolism and an inhibition of autophagy. At the same time, CCL2 would interact with its receptor (CRR2) and present on monocytes, promoting their migration to sites of injury, their differentiation to macrophages, and their synthesis of new ROS, producing a vicious circle that would trigger and aggravate the disease.