Understanding the relationships among prognostic biomarkers of myocardial stress, injury, inflammation, and fibrosis, such as NT-proBNP, troponin, soluble urokinase-type plasminogen activator receptor (suPAR), and Gal-3, can elucidate mechanisms of HF pathogenesis, adverse ventricular remodeling, and key pathways important to disease progression [276]. This evidence concerns the gene LGALS3 and hydrops fetalis.