Clinical research progress of renal denervation for heart failure treatment: current evidence, controversies, and future directions

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  Figure 1. Targeting the vicious cardiorenal sympathetic cycle in heart failure via renal denervation (RDN). (Left panel) The vicious cardiorenal sympathetic cycle. In the setting of heart failure (HF), diminished cardiac output and arterial baroreceptor unloading (arterial baroreflex input from the carotid sinus and aortic arch) trigger a compensatory increase in central sympathetic outflow. Efferent renal sympathetic nerve activity (solid red arrows) is increased, stimulating renin release from juxtaglomerular cells, enhancing tubular sodium reabsorption, and reducing renal blood flow. This leads to activation of the renin-angiotensin-aldosterone system (RAAS) and fluid retention, which further exacerbates cardiac wall stress, oxygen demand, and adverse remodeling. Concurrently, afferent renal sensory nerve signaling (dashed blue arrows) transmits excitatory signals from the kidney to the central nervous system (CNS), further augmenting systemic sympathetic drive. This establishes a deleterious positive feedback loop that accelerates HF progression. (Right panel) Therapeutic mechanisms of renal denervation (RDN). The schematic illustrates disruption of the cardiorenal axis via…