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Pharmacological inhibition of galectin-3 protects against hypertensive nephropathy
Anne-Roos S Frenay1, Lili Yu2, A Rogier van der Velde3
1Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands;
Abstract:
Galectin-3 activation is involved in the pathogenesis of renal damage and fibrogenesis. Limited data are available to suggest that galectin-3-targeted intervention is a potential therapeutic candidate for the prevention of chronic kidney disease. Homozygous TGR(mREN)27 (REN2) rats develop severe high blood pressure (BP) and hypertensive end-organ damage, including nephropathy and heart failure. Male REN2 rats were treated with N-acetyllactosamine [galectin-3 inhibitor (Gal3i)] for 6 wk; untreated REN2 and Sprague-Dawley rats served as controls. We measured cardiac function with echocardiogram and invasive hemodynamics before termination. BP and proteinuria were measured at baseline and at 3 and 6 wk. Plasma creatinine was determined at 6 wk. Renal damage was assessed for focal glomerular sclerosis, glomerular desmin expression, glomerular and interstitial macrophages, kidney injury molecule-1 expression, and α-smooth muscle actin expression. Inflammatory cytokines and extracellular matrix proteinases were quantified by quantitative real-time PCR. Systolic BP was higher in control REN2 rats, with no effect of Gal3i treatment. Plasma creatinine and proteinuria were significantly increased in control REN2 rats; Gal3i treatment reduced both. Renal damage (focal glomerular sclerosis, desmin, interstitial macrophages, kidney injury molecule-1, α-smooth muscle actin, collagen type I, and collagen type III) was also improved by Gal3i. All inflammatory markers (CD68, IL-68, galectin-3, and monocyte chemoattractant protein-1) were elevated in control REN2 rats and attenuated by Gal3i. Markers of extracellular matrix turnover were marginally altered in untreated REN2 rats compared with Sprague-Dawley rats. In conclusion, galectin-3 inhibition attenuated hypertensive nephropathy, as indicated by reduced proteinuria, improved renal function, and decreased renal damage. Drugs binding to galectin-3 may be therapeutic candidates for the prevention of chronic kidney disease.
Insights
Galectin-3 inhibition reduced kidney damage and improved renal function in hypertensive rats. This suggests galectin-3 inhibitors may prevent chronic kidney disease progression.
Area of Science:
- Nephrology
- Cardiovascular Research
- Immunology
Background:
- Galectin-3 plays a role in kidney damage and fibrosis.
- Galectin-3 targeted therapies show potential for preventing chronic kidney disease (CKD).
- Hypertensive TGR(mREN)27 (REN2) rats exhibit severe hypertension and end-organ damage, including nephropathy.
Purpose of the Study:
- To investigate the therapeutic potential of galectin-3 inhibition in hypertensive nephropathy.
- To assess the effects of N-acetyllactosamine (a galectin-3 inhibitor) on renal damage and function in REN2 rats.
Main Methods:
- Male REN2 rats were treated with N-acetyllactosamine (Gal3i) for 6 weeks.
- Cardiac function, blood pressure, proteinuria, and plasma creatinine were measured.
- Renal damage markers, inflammatory cytokines, and extracellular matrix proteins were analyzed.
Main Results:
- Gal3i treatment significantly reduced proteinuria and plasma creatinine levels.
- Renal damage, including focal glomerular sclerosis and interstitial fibrosis, was improved by Gal3i.
- Inflammatory markers (galectin-3, CD68, IL-6, MCP-1) were attenuated by Gal3i treatment.
Conclusions:
- Galectin-3 inhibition effectively attenuated hypertensive nephropathy in REN2 rats.
- Reduced proteinuria, improved renal function, and decreased renal damage indicate therapeutic potential.
- Galectin-3 binding drugs are promising candidates for preventing chronic kidney disease.
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