Galectin-1 Is a Marker but Not a Mediator of Heart Failure With Preserved Ejection Fraction

BACKGROUND: ) is a carbohydrate-binding protein that we previously identified as being upregulated in cardiac myeloid cells in a preclinical model of HFpEF. Our objective was to determine the role of galectin-1 in HFpEF in both preclinical models and clinical cohort studies. METHODS: Galectin-1 was measured using the Olink proximity extension assay in human cohorts. HFpEF was induced in mice with myeloid-specific and global deletion of galectin-1 and corresponding controls using the hypertensive deoxycorticosterone acetate-salt model. RESULTS: <0.001). Mice with myeloid cell or global deficiency of galectin-1, however, exhibit no difference in deoxycorticosterone acetate-salt-induced HFpEF. CONCLUSIONS: Greater circulating galectin-1 levels are associated with a higher risk of incident heart failure and higher NT-proBNP among patients with acute HFpEF. However, neither global nor myeloid deficiency of galectin-1 altered the cardiovascular phenotype in a preclinical model of HFpEF, suggesting that it is a marker but not a causal mediator of the disease.