Background: The aim of the elucidation of mechanisms implicated in the chronification of inflammation
is to shed light on the pathogenesis of disorders that are responsible for the majority of the incidences of
diseases and deaths, and also causes of ageing. Atherosclerosis is an example of the most significant inflammatory
pathology. The inflammatory response of innate immunity is implicated in the development of atherosclerosis
arising locally or focally.
Modified low-density lipoprotein (LDL) was regarded as the trigger for this response. No atherosclerotic changes
in the arterial wall occur due to the quick decrease in inflammation rate. Nonetheless, the atherosclerotic lesion
formation can be a result of the chronification of local inflammation, which, in turn, is caused by alteration of the
response of innate immunity.
Objective: In this review, we discussed potential mechanisms of the altered response of the immunity in atherosclerosis
with a particular emphasis on mitochondrial dysfunctions.
Conclusion: A few mitochondrial dysfunctions can be caused by the mitochondrial DNA (mtDNA) mutations.
Moreover, mtDNA mutations were found to affect the development of defective mitophagy. Modern investigations
have demonstrated the controlling mitophagy function in response to the immune system. Therefore, we
hypothesized that impaired mitophagy, as a consequence of mutations in mtDNA, can raise a disturbed innate
immunity response, resulting in the chronification of inflammation in atherosclerosis.