Shared Mechanisms in Cancer and Cardiovascular Disease: S100A8/9 and the NLRP3 Inflammasome
Sophie Van Linthout
Abstract
Inflammation and a dysregulated immune system are common denominators in cancer and cardiovascular disease (CVD). The Canakinumab Anti-Inflammatory Thrombosis Outcome Study (CANTOS) highlighted the convergence of interleukin (IL)-1β biology in cancer and CVD, and the potential of anti–IL-1β drugs for the treatment of both disease entities. Accumulating evidence further supports the role of the innate immunity members and IL-1β activators, S100A8/9 and the NLRP3 inflammasome, in both cancer and CVD. This review outlines the common involvement of S100A8/9 and the NLRP3 inflammasome, in cancer and CVD. Specifically, their time-, cell-, and context-dependent actions and hereto-related dichotomous role in different cancers and CVD are addressed, highlighting the need for further insights to allow tailored therapies. • S100A8/9 and the NLRP3 inflammasome contribute to both cancer and CVDs. • S100A8/9 and the NLRP3 inflammasome act in a time-, cell-, and context-dependent manner. • S100A8/9 and the NLRP3 inflammasome can be detrimental, but also beneficial in cancer and CVD. • Their dichotomous roles in different cancers and CVD needs further investigation to allow tailored therapies.