Mechanistic intersections of empagliflozin and nebivolol in aging-associated redox and inflammatory pathways
Abstract
Aging is characterized by interconnected disturbances in oxidative stress, chronic inflammation, mitochondrial dysfunction, and nutrient-sensing pathways that collectively contribute to progressive metabolic and vascular decline. Among the central molecular mechanisms implicated in these processes are dysregulation of the AMPK–mTOR–SIRT1 axis, persistent NF-κB activation, impaired Nrf2-mediated antioxidant defense, and mitochondrial redox imbalance. Pharmacological strategies capable of modulating multiple components of this network have therefore gained increasing interest in aging-related research. Empagliflozin, a sodium–glucose cotransporter-2 (SGLT2) inhibitor, has demonstrated pleiotropic metabolic effects extending beyond glycemic control, including modulation of AMPK signaling, attenuation of oxidative stress, and suppression of inflammatory activation. Nebivolol, a third-generation β 1 -selective adrenergic blocker with nitric oxide–mediated vasodilatory properties, has been associated with endothelial protection, vascular redox regulation, and anti-inflammatory activity. Although both agents influence pathways relevant to aging biology, current evidence is derived predominantly from experimental models of cardiovascular or metabolic disease rather than from physiological aging studies. Moreover, direct evidence evaluating their combined effects in aging remains unavailable. This review critically examines the mechanistic roles of empagliflozin and nebivolol within…
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