BACKGROUND AND OBJECTIVE

Interleukin-6 (IL-6) plays multifaceted roles in cancer and atherosclerosis. Initially recognized for its role in immune response and inflammation, IL-6 promotes tumor progression via the JAK-STAT and MAP kinase pathways and is associated with poor cancer prognoses. In atherosclerosis, IL-6 contributes to endothelial dysfunction and plaque formation. This review highlights the shared inflammatory mechanisms of IL-6 in both diseases and explores the regulatory dynamics of IL-6 signaling, including gene polymorphisms and epigenetic modifications.

METHODS

Google Scholar, Scopus, and PubMed were searched for English-language articles on IL-6 and those reporting shared pathogenic mechanisms of IL-6 in cancer and atherosclerosis from their inception through June 2024.

KEY CONTENT AND FINDINGS

The investigation into IL-6's mechanisms in cancer and atherosclerosis reveals the intricate and interconnected nature of inflammatory processes in chronic diseases. The role of IL-6 in both conditions underscores its centrality in disease pathology, particularly through its involvement in inflammation, immune modulation, and cellular proliferation. This commonality highlights IL-6 as a key player linking these seemingly distinct diseases.

CONCLUSIONS

Given the shared pathogenic mechanism of IL-6 in cancer and atherosclerosis, this narrative review concludes by emphasizing the therapeutic potential of modulating IL-6 in treating both cancer and atherosclerosis. It advocates for personalized treatment strategies that combine targeted therapies with lifestyle modifications. This holistic approach is considered crucial for effective disease management, given the diverse and complex roles IL-6 plays in these widespread conditions.