Galectin-3 in Renal Pathology: More Than Just an Innocent Bystander?

Desmedt, Valérie; Desmedt, Stéphanie; Delanghe, Joris; Speeckaert, Reinhart; Speeckaert, Marijn M.

doi:10.1159/000446376

Cited by 70 publications

(58 citation statements)

References 91 publications

(113 reference statements)

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“…Higher concentrations of Gal-3 may be associated with progression of CKD, indicating potential novel mechanisms related to Gal-3 expression that may contribute to the progression of CKD [25]. Furthermore, Gal-3 is reported to play a pivotal role in renal interstitial fibrosis and progression of CKD [117]. Thus, inhibition of Gal-3 may be a promising therapeutic strategy to prevent advanced renal disease.…”

Section: Gal-3 As a Biomarker Of Ckd In Clinical Studiesmentioning

confidence: 99%

Galectin-3 as a Next-Generation Biomarker for Detecting Early Stage of Various Diseases

et al. 2020

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Galectin-3 is a β-galactoside-binding lectin which is important in numerous biological activities in various organs, including cell proliferation, apoptotic regulation, inflammation, fibrosis, and host defense. Galectin-3 is predominantly located in the cytoplasm and expressed on the cell surface, and then often secreted into biological fluids, like serum and urine. It is also released from injured cells and inflammatory cells under various pathological conditions. Many studies have revealed that galectin-3 plays an important role as a diagnostic or prognostic biomarker for certain types of heart disease, kidney disease, viral infection, autoimmune disease, neurodegenerative disorders, and tumor formation. In particular, it has been recognized that galectin-3 is extremely useful for detecting many of these diseases in their early stages. The purpose of this article is to review and summarize the recent literature focusing on the biomarker characteristics and long-term outcome predictions of galectin-3, in not only patients with various types of diseases, but associated animal models.

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Section: Gal-3 As a Biomarker Of Ckd In Clinical Studiesmentioning

confidence: 99%

Galectin-3 as a Next-Generation Biomarker for Detecting Early Stage of Various Diseases

et al. 2020

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“…Thus, the ability to cleave galectin-3 appears to be a preserved function in adherent staphylococcal species; both S. epidermidis and S. aureus form biofilms on medical devices (2,5), and it may be hypothesized that galectin-3 processing is associated not only with superficial skin infection but also with graft-related infection. S. saprophyticus, commonly causing urinary tract infection, lacked galectin-3-processing capacity even though galectin-3 is present throughout the urinary tract (46), in line with the lack of any known exoprotease expression in this species (47).…”

Section: Discussionmentioning

confidence: 81%

Galectin-3 Is a Target for Proteases Involved in the Virulence of Staphylococcus aureus

Elmwall

Kwieciński

et al. 2017

Infect Immun

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Staphylococcus aureus is a major cause of skin and soft tissue infection. The bacterium expresses four major proteases that are emerging as virulence factors: aureolysin (Aur), V8 protease (SspA), staphopain A (ScpA), and staphopain B (SspB). We hypothesized that human galectin-3, a ␤-galactoside-binding lectin involved in immune regulation and antimicrobial defense, is a target for these proteases and that proteolysis of galectin-3 is a novel immune evasion mechanism. Indeed, supernatants from laboratory strains and clinical isolates of S. aureus caused galectin-3 degradation. Similar proteolytic capacities were found in Staphylococcus epidermidis isolates but not in Staphylococcus saprophyticus. Galectin-3-induced activation of the neutrophil NADPH oxidase was abrogated by bacterium-derived proteolysis of galectin-3, and SspB was identified as the major protease responsible. The impact of galectin-3 and protease expression on S. aureus virulence was studied in a murine skin infection model. In galectin-3 ϩ/ϩ mice, SspB-expressing S. aureus caused larger lesions and resulted in higher bacterial loads than protease-lacking bacteria. No such difference in bacterial load or lesion size was detected in galectin-3 Ϫ/Ϫ mice, which overall showed smaller lesion sizes than the galectin-3 ϩ/ϩ animals. In conclusion, the staphylococcal protease SspB inactivates galectin-3, abrogating its stimulation of oxygen radical production in human neutrophils and increasing tissue damage during skin infection.

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“…As a member of an evolutionarily conserved family of soluble β‐galactoside‐binding lectins, galectin‐3 is associated with the activation of macrophages and fibroblasts, which leads to inflammation and fibrosis . In the kidney, galectin‐3 is mainly expressed in epithelial cells in glomerular mesangium, distal tubules and proximal tubules . Pugliese et al has found that galectin‐3 could protect kidney from advanced glycosylation end products‐induced renal tissue injury in diabetic mice .…”

Section: Discussionmentioning

confidence: 99%

Elevated High Sensitivity C‐Reactive Protein Increases the Risk of Microalbuminuria in Subjects With Cardiovascular Disease Risk Factors

Yang

Liu

et al. 2017

Ther Apher Dial

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Microalbuminuria is an early biomarker of kidney injury, the aim of this study was to investigate the impact of high sensitivity C-reactive protein (hs-CRP) on microalbuminuria in adults with cardiovascular disease (CVD) risk factors. A total of 5667 subjects who voluntarily attended annual health screenings in the Third Xiangya Hospital of Central South University were included in the study. Logistic regression was used to determine the validity of hs-CRP to predict the presence of microalbuminuria. In the unadjusted regression analysis, male gender (OR 2.23), age (OR 1.71), smoking status (OR 1.48), obesity (OR 2.41), hypertension(OR 4.03), diabetes (OR 4.61), hyperuricemia (OR 1.83), and high hs-CRP(OR 1.61) were associated with microalbuminuria. Multivariate logistic regression analysis showed that the adjusted odds ratios (OR) of diabetes, hypertension, male, abdominal obesity, and high hs-CRP for microalbuminuria were 2.71, 2.57, 1.51, 1.28 and 1.41 in all subjects, respectively (P < 0.01). ROC analysis indicated that the cut-off for hs-CRP with better properties for screening of microalbuminuria was identified as ≥0.85 mg/L. The ORs of microalbuminuria were 1.97, 1.49, 1.32 and 1.71 times in male, abdominal obesity, diabetes and hypertension subjects with hs-CRP ≥ 0.85 mg/L, respectively, compared with those without elevated hs-CRP (P < 0.01). Elevated hs-CRP level was associated with microalbuminuria independent of cardiovascular risk factors. In addition, elevated hs-CRP increased the risk of developing microalbuminuria in subjects with CVD risk factors, indicating that chronic inflammation could amplify the deterioration of kidney by effect of CVD risk factors.

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Galectin-3 in Renal Pathology: More Than Just an Innocent Bystander?

Cited by 70 publications

References 91 publications

Galectin-3 as a Next-Generation Biomarker for Detecting Early Stage of Various Diseases

Galectin-3 as a Next-Generation Biomarker for Detecting Early Stage of Various Diseases

Galectin-3 Is a Target for Proteases Involved in the Virulence of Staphylococcus aureus

Elevated High Sensitivity C‐Reactive Protein Increases the Risk of Microalbuminuria in Subjects With Cardiovascular Disease Risk Factors

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