ArticleThe American journal of pathology2006
Galectin-3 associates with the primary cilium and modulates cyst growth in congenital polycystic kidney disease.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- A cross-model single-cell atlas reveals conserved involvement of osteopontin in polycystic kidney disease.JCI insight · 2026Article
- A cross model spatial and single-cell atlas reveals the conserved involvement of osteopontin in polycystic kidney disease.bioRxiv : the preprint server for biology · 2025Article
- Galectin-3 induces neurodevelopmental apical-basal polarity and regulates gyrification.Science advances · 2025Article
- Reduction of elevated Gli3 does not alter the progression of autosomal recessive polycystic kidney disease.Physiological reports · 2025Article
- Galectin-3: action and clinical utility in chronic kidney disease.International urology and nephrology · 2024Review
- Evaluation of galectin-3 and intestinal fatty acid binding protein as serum biomarkers in autosomal recessive polycystic kidney disease.Journal of nephrology · 2023Article
- Galectin-3 in Kidney Diseases: From an Old Protein to a New Therapeutic Target.International journal of molecular sciences · 2022Review
- Galectin-3-A New Player of Kidney Damage or an Innocent Bystander in Children with a Single Kidney?Journal of clinical medicine · 2021Article
- STAT signaling in polycystic kidney disease.Cellular signalling · 2020Review
- Targeting and therapeutic peptide-based strategies for polycystic kidney disease.Advanced drug delivery reviews · 2020Review
- Identification of targets of IL-13 and STAT6 signaling in polycystic kidney disease.American journal of physiology. Renal physiology · 2018Article
- Spindle pole cohesion requires glycosylation-mediated localization of NuMA.Scientific reports · 2017Article
- Cardiac dysfunction in Pkd1-deficient mice with phenotype rescue by galectin-3 knockout.Kidney international · 2016Article
- Vascular Endothelial Growth Factor C for Polycystic Kidney Diseases.Journal of the American Society of Nephrology : JASN · 2016Article
- Basal foot MTOC organizes pillar MTs required for coordination of beating cilia.Nature communications · 2014Article
- Review
- Expression of Fraser syndrome genes in normal and polycystic murine kidneys.Pediatric nephrology (Berlin, Germany) · 2012Article
- Galectin-7 modulates the length of the primary cilia and wound repair in polarized kidney epithelial cells.American journal of physiology. Renal physiology · 2011Article
- Modified citrus pectin reduces galectin-3 expression and disease severity in experimental acute kidney injury.PloS one · 2011Article
- Differential expression of renal proteins in a rodent model of Meckel syndrome.Nephron. Experimental nephrology · 2011Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
Several lines of evidence implicate the beta-galactoside-binding lectin galectin-3 in development and pathological processes in renal collecting ducts: galectin-3 is expressed in the ureteric bud/collecting duct lineage during nephrogenesis, modulates collecting duct growth/differentiation in vitro, and is expressed in human autosomal recessive polycystic kidney disease in cyst epithelia, almost all of which arise from collecting ducts. Moreover, exogenous galectin-3 restricts growth of cysts generated by Madin-Darby canine kidney collecting duct-derived cells in three-dimensional culture in collagen. Using the cpk mouse model of recessively inherited polycystic kidney disease, we observed widespread galectin-3 mRNA and protein in cyst epithelia. Exogenous galectin-3 reduced cyst formation in suspension culture, and mice-null mutant for galectin-3 had more extensive renal cysts in vivo. Galectin-3 was also detected for the first time in the centrosome/primary cilium, which has been implicated in diverse polycystic kidney disease. Cilia structure/number appeared normal in galectin-3-null mutants. Finally, paclitaxel, a therapy that retards polycystic kidney disease in cpk mice, increased extracellular galectin-3, in which the lectin could potentially interact with cilia. These data raise the possibility that galectin-3 may act as a natural brake on cystogenesis in cpk mice, perhaps via ciliary roles.
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Registered trials
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