| Title: | Galectin-1 Is a Marker but Not a Mediator of Heart Failure With Preserved Ejection Fraction |
| Journal: | Hypertension |
| Published: | 30 Jan 2026 |
| Pubmed: | https://pubmed.ncbi.nlm.nih.gov/41614247/ |
| DOI: | https://doi.org/10.1161/hypertensionaha.125.26006 |
| URL: | https://pmc.ncbi.nlm.nih.gov/articles/PMC12879785/ |
Publication 18414
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Abstract
BACKGROUND: The immune system is emerging as a key player in driving cardiac remodeling in heart failure with preserved ejection fraction (HFpEF). Galectin-1 (Lgals1) 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.</p>
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.</p>
RESULTS: Plasma galectin-1 was higher in both a preclinical model of HFpEF (P=0.022) and in patients with heart failure (P<0.001) in the UK Biobank. In patients without heart failure, higher galectin-1 levels were associated with a greater risk for incident heart failure (hazard ratio, 3.1 for quartile 4 versus quartile 1; P<0.001). In patients with acute HFpEF, galectin-1 was positively associated with NT-proBNP (N-terminal pro-B-type natriuretic peptide), a biomarker of worse prognosis (ordinal regression P<0.001). Mice with myeloid cell or global deficiency of galectin-1, however, exhibit no difference in deoxycorticosterone acetate-salt-induced HFpEF.</p>
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.</p>
12 Keywords
- Aged
- Animals
- Biomarkers
- Disease Models, Animal
- Female
- Galectin 1
- Heart Failure
- Humans
- Male
- Mice
- Middle Aged
- Stroke Volume
15 Authors
- Jean W. Wassenaar
- C. Duncan Smart
- Daniel J. Fehrenbach
- Megan M. Shuey
- Pranoy Sangowdar
- Lin Zhong
- Francis J. Miller
- Quinn S. Wells
- Shi Huang
- Sean P. Collins
- Alan B. Storrow
- Karen F. Miller
- Deepak K. Gupta
- Amanda C. Doran
- Meena S. Madhur
1 Application
| Application ID | Title |
|---|---|
| 57492 | Resolving the genetic architecture of complex cardiovascular disease through phenotype refinement. |
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