Common Pathophysiological Mechanisms Connecting Dyslipidemia and Hyperuricemia: a Narrative Review

This review presents the pathophysiological changes underlying dyslipidemia and hyperuricemia. The way in which these health conditions influence each other is through insulin resistance, persistent inflammatory state, oxidative stress and endothelial damage. Insulin resistance influences lipid metabolism and uric acid elimination, leading to triglyceride accumulation and increased uric acid levels. Inflammatory mediators in adipose tissue and cytokine cascades maintain an inflammatory status, favor lipid peroxidation and decrease renal uric acid clearance. Reactive oxygen species amplified by oxidized lipoproteins and urate compromise nitric oxide signaling pathways and vascular homeostasis. Genetic and epigenetic alterations in genes involved in metabolic transport, cytokine regulation and microRNA expression also occur. This dual pathology favors vascular vulnerability and systemic metabolic dysregulation. Effective management requires more than simple monitoring of serum markers. This should target the molecular mechanisms that fuel cardiovascular and metabolic damage.