Figure 1.

The model of atherosclerosis development due to chronic inflammation induced by a combination of recognition errors of modified low-density lipoproteins (LDLs) as pathogens and impaired mitophagy. Modified LDLs form self-associates and are identified by arterial cells as pathogens. After phagocytosis of LDL associates, a moderate inflammatory response is activated, leading to moderate intracellular lipid accumulation and moderate atherogenesis and the damage can still be repaired. However, in case of impaired mitophagy due to mitochondrial mutations, the inflammatory response, once being activated by modified LDL, does not stop and the inflammation becomes uncontrollable, leading to massive intracellular lipids accumulation, infiltration of immune cells, and strong atherogenesis. Modified and adapted from [15].