Neurohormonal Pathways in Heart Failure: New Targets for Therapy

Heart failure is fundamentally driven by maladaptive activation of neurohormonal systems, including the renin–angiotensin–aldosterone system (RAAS), the sympathetic nervous system, and natriuretic peptide pathways. These cascades orchestrate fluid retention, vasoconstriction, and ventricular remodeling, ultimately worsening cardiac dysfunction. Over the past decades, therapies such as ACE inhibitors, beta-blockers, and mineralocorticoid receptor antagonists have revolutionized patient outcomes by targeting these pathways. However, despite these advances, morbidity and mortality in heart failure remain high, underscoring the need to explore novel targets within the neurohormonal network.

Emerging research is focusing on previously underexplored mediators such as neprilysin, endothelin, adenosine, and guanylyl cyclase pathways. The introduction of angiotensin receptor–neprilysin inhibitors (ARNIs) demonstrated the transformative potential of dual pathway modulation, while soluble guanylyl cyclase stimulators and endothelin antagonists are under clinical investigation. Understanding cross-talk between these systems and integrating multi-target approaches holds promise for precision therapies. This track will highlight cutting-edge strategies aimed at refining neurohormonal blockade, identifying new druggable pathways, and personalizing treatment for diverse patient subgroups.

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