ReviewFrontiers in cardiovascular medicine2026
IL-18 in atherosclerosis: context-dependent biology, human evidence, and translational challenges.
Review in Frontiers in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Atherosclerosis is a chronic inflammatory disease shaped by interactions among vascular cells, innate immunity, adaptive immunity, and metabolic stress. Interleukin-18 (IL-18), an IL-1 superfamily cytokine activated predominantly downstream of inflammasomes, links vascular injury to type 1 immune responses. This structured narrative review integrates mechanistic, plaque-tissue, epidemiological, genetic, and therapeutic evidence for IL-18 in atherosclerosis. Experimental studies generally support pro-atherogenic actions, but these effects vary by plaque stage, cellular context, and genetic background. Human studies consistently show enrichment of IL-18 in inflamed plaques, whereas circulating IL-18 has limited independent diagnostic or prognostic performance after multivariable adjustment in several large cohorts. Drug-target Mendelian randomization supports associations with selected cardiovascular outcomes, but does not substitute for randomized clinical evidence and remains vulnerable to pleiotropy, instrument strength, ancestry, and lifelong-exposure assumptions. Direct IL-18 inhibitors have entered clinical development in inflammatory diseases, yet cardiovascular outcome efficacy has not been established. We therefore position IL-18 as a biologically plausible but unvalidated cardiovascular target and outline a stage-gated translational agenda centered on free IL-18 assays, plaque-context biomarkers, pharmacology, patient selection, and long-term safety.
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