ReviewFrontiers in immunology2026
Aging-driven metabolic abnormalities remodel intercellular communication through the gut-liver-heart axis and may promote coronary artery disease: the key role of bile acid metabolism.
Review in Frontiers in immunology, 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
Coronary artery disease (CAD) remains the leading cause of cardiovascular mortality worldwide and shows a strong age-dependence that classical risk-factor models do not fully explain. A growing body of work indicates that aging is closely associated with CAD and, in preclinical models, can promote it through immunometabolic remodeling of the gut-liver-heart axis, in which bile acid metabolism is proposed to act as a central molecular link. Here we integrate cellular, molecular, and clinical evidence to outline how aging perturbs this axis and sustains chronic vascular inflammation. At the cellular level, senescent cells in the intestinal, hepatic, and vascular compartments generate the senescence-associated secretory phenotype (SASP) - a process linked to cGAS-STING and NLRP3 inflammasome activation, mitochondrial dysfunction, and decline of the NAD
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