ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Macrophage Derived Galectin-3 Promotes Renal Fibrosis and Diabetic Kidney Disease by Enhancing TGFβ1 Signaling.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The lactate-lactylation axis in renal fibrosis: potential mechanisms in diabetic kidney disease.Annals of medicine · 2025Pooled it
- Macrophage FOXO1 Inhibition Protects Against Hyperglycaemia-Associated Kidney Injury.Basic & clinical pharmacology & toxicology · 2026Article
- Macrophage-Fibroblast Crosstalk in Kidney Injury: A Narrative Review.International journal of molecular sciences · 2026Review
- Spatial multi omic profiling maps hypoxia-driven pro-fibrotic SPP1Experimental hematology & oncology · 2026Article
- Expression, Localization and Actions of Galectin-3: Implications in the Pathophysiology and Therapy of Cardiovascular Disease.International journal of molecular sciences · 2026Review
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Modified citrus pectin modulates splenic immune responses and galectin expression following cisplatin treatment in Wistar rats.Journal of molecular histology · 2026Article
- Galectin-3 Promotes Graft Injury via NLRP3 Pyroptosis in Steatotic Liver Transplantation: A Therapeutic Target for Donor Optimization.Journal of clinical and translational hepatology · 2026Article
- Galectin-3 and Cardio-Kidney Outcomes: A Bit of History Repeating.Kidney medicine · 2026Article
- Metabolic Reprogramming and Immunometabolic Dysregulation in Diabetic Kidney Disease: From Pathogenesis to Precision Multi-target Therapies.Research (Washington, D.C.) · 2026Review
- Modulating Renal Fibrosis: The Emerging Role of Hepatocyte Growth Factor.International journal of nephrology · 2026Review
- An intricate relationship between fibrosis and autoimmune diseases: a specific focus on unraveling its molecular, immunological, and epigenetic drivers.Frontiers in immunology · 2026Review
- RP-182 alleviated obstruction-induced renal fibrosis by reprogramming CD206Frontiers in pharmacology · 2026Article
- Regulatory networks of post-translational modifications in diabetic kidney disease: from pathogenic mechanisms to therapeutic frontiers.Frontiers in endocrinology · 2026Review
- Metabolic reprogramming in diabetic complications: mechanisms, pathologies, and molecular evidence from multi-organ studies.Frontiers in immunology · 2026Review
- Mechanisms of Macrophage Glycolytic Reprogramming and Interventional Effects of Traditional Chinese Medicine on Renal Fibrosis.International journal of general medicine · 2026Review
- Galectin-3 and the Glyco-Inflammatory Axis: A Missing Link to Residual Cardiovascular Risk in Coronary Artery Disease.Biomedicines · 2025Review
- Macrophage Derived Galectin-3 Promotes Renal Fibrosis and Diabetic Kidney Disease by Enhancing TGFβ1 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
18 authors.
Funding
Abstract
Over 30% of patients with type 2 diabetes develop diabetic kidney disease (DKD), which has emerged as a major contributor to end stage renal disease. Renal fibrosis represents the final pathological outcome of most chronic kidney disease, particularly DKD. This study demonstrates elevated levels of Galectin-3 (Gal3), a lectin associated with inflammatory and fibrotic conditions, in the plasma and kidneys of DKD mice. Positive correlations between Gal3 expression and renal fibrosis are observed in both DKD patients and mice. Macrophage-derived Gal3 is found to promote Transforming growth factor beta 1 (TGFβ1) signaling activation and renal fibrogenesis. Genetic ablation of Gal3 globally or specifically in macrophages, as well as pharmacological inhibition of Gal3, significantly attenuated kidney fibrosis in diabetic mice. Mechanistically, macrophage-derived Gal3 interacted with TGFβ receptor2 (TGFBR2) and Pro-TGFβ1, preventing TGFBR2 proteasomal degradation in fibroblasts and increasing TGFβ1 levels in the diabetic kidney. These events enhances TGFβ1 signaling activation and ultimately facilitated kidney fibrosis. The findings of this study suggest Gal3 as a potential therapeutic target for renal fibrosis and DKD.
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