Inflammation as the Central Integrator of Cardiometabolic and Chronic Disease Pathophysiology

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Abstract
Systemic low-grade inflammation has emerged as a central biological mechanism underlying the development and progression of major chronic non-communicable diseases. This integrative review analyzes mechanistic, epidemiological, and interventional evidence supporting inflammation as a unifying pathophysiological axis, with particular emphasis on cardiovascular disease. Foundational immunological frameworks describe nonresolving inflammation as a driver of endothelial dysfunction, cytokine amplification, metabolic dysregulation, and tissue remodeling. In atherosclerotic cardiovascular disease, inflammatory signaling within the arterial wall contributes to plaque instability and thrombo-inflammatory activation, and clinical trial data demonstrate that targeted anti-inflammatory therapy can reduce recurrent cardiovascular events in selected populations. Parallel evidence from immunometabolic research links obesity and type 2 diabetes to chronic inflammatory activation, reinforcing the interconnected immune–metabolic–vascular model. The review also addresses inflammaging and multimorbidity, highlighting how sustained inflammatory tone increases vulnerability to cardiometabolic and systemic disease across the lifespan. Translational implications include biomarker-guided risk stratification, recognition of residual inflammatory risk, and integration of lifestyle and pharmacologic strategies aimed at modulating inflammatory burden. From an international perspective, particularly in middle-income countries experiencing epidemiological transition, understanding systemic inflammation as a shared biological substrate may support more integrated prevention and management strategies within internal medicine.