Abstract
Inflammation is a key process in metazoan organisms due to its relevance for innate defense against infections and tissue damage. However, inflammation is also implicated in pathological processes such as atherosclerosis. Atherosclerosis is a chronic inflammatory disease of the arterial wall where unstable atherosclerotic plaque rupture causing platelet aggregation and thrombosis may compromise the arterial lumen, leading to acute or chronic ischemic syndromes. In this review, we will focus on the role of mitochondria in atherosclerosis while keeping inflammation as a link. Mitochondria are the main source of cellular energy. Under stress, mitochondria are also capable of controlling inflammation through the production of reactive oxygen species (ROS) and the release of mitochondrial components, such as mitochondrial DNA (mtDNA), into the cytoplasm or into the extracellular matrix, where they act as danger signals when recognized by innate immune receptors. Primary or secondary mitochondrial dysfunctions are associated with the initiation and progression of atherosclerosis by elevating the production of ROS, altering mitochondrial dynamics and energy supply, as well as promoting inflammation. Knowing and understanding the pathways behind mitochondrial-based inflammation in atheroma progression is essential to discovering alternative or complementary treatments.
Highlights
Enhanced reactive oxygen species (ROS) production causes endothelial dysfunction, vascular inflammation, and accumulation of oxidized LDLs (oxLDLs) in the arterial wall, which are responsible for the formation of the early plaque and its growth [96]. These findings indicate that mitochondrial dysfunction, in combination with oxLDL, originates a continuous cycle associated with inflammation that will eventually lead to atheroma formation
Atherosclerosis is considered an inflammatory disease in which mitochondrial dysfunction may play an essential role
The most studied inflammatory process in atherosclerosis is related with NLRP3 inflammasome
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Pattern recognition receptors (PRRs), including Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), NOD-like receptors (NLRs), and C-type lectin receptors (CLRs), are sensors that recognize both PAMPs and DAMPs. The ligation of PRRs by DAMPs induces intracellular signaling pathways that promote the expression and activation of several pro-inflammatory mechanisms whose regulation and response depend on the PRR and cell. MtDNA is released by damaged cells and can be sensed by a PRR, the Toll-like receptor 9 (TLR9), which is the receptor for CpG motifs in DNA [16] This interaction leads to the NF-κB activation signaling pathway and, the induction of multiple pro-inflammatory genes [17,18]. Mitochondria are highly related to many inflammatory pathways, in this review, we will focus on NLRP3 activation, since it has proven to be a key event in the inflammatory process of atherosclerosis [28] and its relationship with mitochondria [29]
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