The connection of systemic inflammation and atherosclerosis: What do we know nowadays?

OBJECTIVE

Aim: To summarise what is known about the inflammatory nature of atherosclerosis to date.

PATIENTS AND

METHODS

Materials and

Methods

We conducted the search using Google Scholar and Medline and selected state-of-the-art articles that were consistent with the aim of study.

CONCLUSION

Conclusions

To date, there is sufficient evidence that atherosclerosis is driven by the inflammatory process. Evidence suggests that atherosclerosis is fundamentally an inflammatory disease, with local systemic inflammation and both being a key drivers of plaque formation and progression. It involves multiple inflammatory mechanisms at all stages, including multiple inflammatory mediators and cytokines (such as IL-1β, IL-6, and TNF-α), CD4+ and CD8+ T-lymphocytes, B-lymphocytes and their subtypes, multiple modes of macrophage activation (including NF-κB-mediated), and neutrophils that undergo NETosis, which exacerbates and builds up inflammation. Inflammatory processes are involved in both plaque formation and plaque destabilization leading to rupture and subsequent thrombosis. Many of these mechanisms have been shown to be applicable as biomarkers of the atherosclerotic process, its severity and its risk level. Currently, a number of antiatherosclerotic therapies targeting inflammation have been developed, but most have not yet been introduced into general medical practice. There is a need to increase awareness of the inflammatory mechanisms underlying atherosclerosis and to apply the knowledge gained in this area to improve the diagnosis, risk stratification and prevention or treatment of this pathology.