ArticleThe American journal of pathology2013
Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.
- Rare genetic variants involved in increased risk of paroxysmal atrial fibrillation in a Japanese population.Scientific reports · 2025Pooled it
- Healing mechanisms of Galectin-1 in the ischemic heart.Cell biochemistry and biophysics · 2026Review
- Galectin-1 Is a Marker but Not a Mediator of Heart Failure With Preserved Ejection Fraction.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Review
- Specialized pro-resolving mediators in myocardial infarction: orchestrators of inflammation resolution and tissue repair.Frontiers in cardiovascular medicine · 2026Review
- Galectin-1 in Cardiovascular Pathogenesis: Unraveling Dual Roles and Mechanistic Insights in Emerging Research.Medicina (Kaunas, Lithuania) · 2025Review
- Probing the CabioRxiv : the preprint server for biology · 2025Article
- Targeting Lactic Acid Modification in Ischemic Heart Diseases: Novel Therapeutics and Mechanism.Journal of cardiovascular translational research · 2025Review
- Galectin-1 correlates with inflammatory markers and T regulatory cells in children with type 1 diabetes and/or celiac disease.Clinical and experimental immunology · 2024Article
- Galectin from Trichinella spiralis alleviates DSS-induced colitis in mice by regulating the intestinal microbiota.Veterinary research · 2024Article
- Understanding the Role of Galectin-1 in Heart Failure: A Comprehensive Narrative Review.Current cardiology reviews · 2024Review
- Pre-treatment with galectin-1 attenuates lipopolysaccharide-induced myocarditis by regulating the Nrf2 pathway.European journal of histochemistry : EJH · 2023Article
- Distinct longevity mechanisms across and within species and their association with aging.Cell · 2023Article
- Matricellular proteins in atherosclerosis development.Matrix biology : journal of the International Society for Matrix Biology · 2023Review
- Targeting galectin-driven regulatory circuits in cancer and fibrosis.Nature reviews. Drug discovery · 2023Review
- Renal Assessment in Acute Cardiorenal Syndrome.Biomolecules · 2023Review
- Modulation of CaHandbook of experimental pharmacology · 2023Article
- Galectin functions in cancer-associated inflammation and thrombosis.Frontiers in cardiovascular medicine · 2023Review
- The interplay of galectins-1, -3, and -9 in the immune-inflammatory response underlying cardiovascular and metabolic disease.Cardiovascular diabetology · 2022Review
- CD69 expression on regulatory T cells protects from immune damage after myocardial infarction.The Journal of clinical investigation · 2022Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 4 countries.
Funding
Abstract
Galectin-1 (Gal-1), an evolutionarily conserved β-galactoside-binding lectin, plays essential roles in the control of inflammation and neovascularization. Although identified as a major component of the contractile apparatus of cardiomyocytes, the potential role of Gal-1 in modulating heart pathophysiology is uncertain. Here, we aimed to characterize Gal-1 expression and function in the infarcted heart. Expression of Gal-1 was substantially increased in the mouse heart 7 days after acute myocardial infarction (AMI) and in hearts from patients with end-stage chronic heart failure. This lectin was localized mainly in cardiomyocytes and inflammatory infiltrates in peri-infarct areas, but not in remote areas. Both simulated hypoxia and proinflammatory cytokines selectively up-regulated Gal-1 expression in mouse cardiomyocytes, whereas anti-inflammatory cytokines inhibited expression of this lectin or had no considerable effect. Compared with their wild-type counterpart, Gal-1-deficient (Lgals1(-/-)) mice showed enhanced cardiac inflammation, characterized by increased numbers of macrophages, natural killer cells, and total T cells, but reduced frequency of regulatory T cells, leading to impaired cardiac function at baseline and impaired ventricular remodeling 7 days after nonreperfused AMI. Treatment of mice with recombinant Gal-1 attenuated cardiac damage in reperfused AMI. Taken together, our results indicate a protective role for Gal-1 in normal cardiac homeostasis and postinfarction remodeling by preventing cardiac inflammation. Thus, Gal-1 treatment represents a potential novel strategy to attenuate heart failure in AMI.
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