Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17931 (galectin-3)
 2,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kidney malformations are common causes of chronic renal failure in children. Dysplastic kidneys represent a unique model of perturbed epithelial-mesenchymal interaction which leads to the formation of malformed branching tubules surrounded by undifferentiated and metaplastic mesenchymal cells. We have found that human dysplastic epithelia express PAX2 (a transcription factor), BCL2 (a survival factor) and galectin-3 (a cell adhesion/signaling molecule). These genes are implicated in oncogenesis and their persistent expression may drive proliferation of dysplastic cysts, hence explaining the massive growth of some multicystic dysplastic kidneys. We have also detected prominent apoptosis in undifferentiated tissues around dysplastic epithelia, and this may provide a potential mechanism for the well-documented regression of dysplastic kidneys. Hence, although these kidneys may not have any excretory function, it is incorrect to consider them as 'end stage organs' because they are highly active in terms of cell turnover and gene expression; furthermore, these processes can be correlated with patterns of tissue growth and involution. Further elucidation of 'molecular lesions' in renal malformations may lead to novel therapies to enhance the differentiation of progenitor cells.
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PMID:Gene expression and cell turnover in human renal dysplasia. 1066 6

Background: Cerebrovascular and cardiovascular diseases contribute substantially to the mortality of end-stage renal disease patients. We sought to combine pulse wave velocity (PWV) with galectin-3 to predict the mortality and cerebrovascular and cardiovascular events in hemodialysis patients. Methods and Results: End-stage renal disease patients who underwent stable hemodialysis were screened for inclusion. Patients with preexisting cardiovascular and cerebrovascular diseases were excluded. The primary endpoint was a composite of all-cause mortality and major adverse cerebrovascular and cardiovascular events. Receiver operating characteristic curve analysis was used to determine the optimal cutoffs to dichotomize PWV and galectin-3. The study population was then stratified into four groups based on these cutoffs. Both univariable and multivariable Cox regression analyses were performed to estimate the hazard ratio and 95% confidence interval (CI) for clinical factors. Model performance was compared among models with or without PWV and galectin-3. A total of 284 patients were enrolled. During a median follow-up of 31 months, 57 patients (20.1%) reached the primary endpoint. The optimal cutoffs for PWV and galectin-3 were 7.9 m/s and 30.5 ng/ml, respectively. In the multivariable regression analysis, the high PWV-high galectin-3 group was associated with a 3-fold increased risk of all-cause mortality and major adverse cerebrovascular and cardiovascular events (hazard ratio = 3.19, 95% CI: 1.05-9.66, p = 0.04) compared with the low PWV-low galectin-3 group. The combination of PWV and galectin-3 was associated with improved model discrimination, calibration, and reclassification. Conclusions: The combination of PWV and galectin-3 can be used to predict mortality and cerebral and cardiovascular complications in hemodialysis patients.
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PMID:Combining Pulse Wave Velocity With Galectin-3 to Predict Mortality and Cerebrovascular and Cardiovascular Events in Hemodialysis Patients. 3319 27