The Inflammatory Axis in Atherosclerosis: Beyond Cholesterol
The management of atherosclerotic cardiovascular disease (ASCVD) has historically focused on the cholesterol hypothesis, emphasizing the reduction of low-density lipoprotein cholesterol (LDL-C). However, even when LDL-C levels are aggressively lowered, a significant residual risk remains. Current evidence increasingly points to systemic inflammation as a central driver of this residual risk. Specifically, the interleukin-1 (IL-1) to interleukin-6 (IL-6) to C-reactive protein (CRP) signaling pathway has emerged as a critical mediator of plaque progression and rupture. While previous trials like CANTOS (targeting IL-1β) provided proof of concept for anti-inflammatory therapy, the medical community is now focusing on IL-6, a more distal and potentially more specific target in the inflammatory cascade.
