Cardiorenal syndrome (CRS) has traditionally been explained through hemodynamic and neurohormonal mechanisms; however, emerging evidence highlights a critical role for immune-metabolic signaling. Osteopontin (OPN), a damage-associated molecular pattern released from injured renal tubular cells, functions as a circulating alarmin that drives inter-organ communication. Renal-derived OPN promotes cardiac fibrosis, metabolic reprogramming, and diastolic dysfunction by suppressing fatty acid oxidation and enhancing glycolysis. Simultaneously, it contributes to pulmonary endothelial injury and inflammation, establishing a kidney-heart-lung axis of dysfunction. The kidney-heart-lung axis refers to the interconnected inflammatory and metabolic communication between injured renal tissue and distant cardiac and pulmonary organs. Elevated circulating OPN correlates with adverse clinical outcomes, underscoring its potential as both a biomarker and therapeutic target in cardiorenal disease progression.
Sarvesh Sabarathinam (Mon,) studied this question.
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