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)

The clinical syndrome of heart failure is characterized by a systemic inflammatory response that contributes to end organ damage in the heart and circulation and can thus lead to worsening heart failure. The ensemble of inflammatory mediators that have been detected in heart failure patients include pro-inflammatory cytokines and their cognate receptors, as well as molecules secreted/released by macrophages (galectin-3 and pentraxin-3). Inflammatory biomarkers correlate with disease severity and prognosis across the broad spectrum of heart failure syndromes. Given the proliferation of new biomarkers that predict disease severity and prognosis in heart failure, it is reasonable to ask whether there is a current role for measuring inflammatory mediators in heart failure. This review will attempt to address this question, as well as review several novel approaches that have utilized inflammatory biomarkers to enhance risk stratification and prognosis in heart failure patients.
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PMID:Positioning of inflammatory biomarkers in the heart failure landscape. 2366 8

Existing diagnostic guidelines for heart failure with preserved ejection fraction (HFPEF) primarily comprise natriuretic peptides and echocardiographic assessment, highlighting the role of diastolic dysfunction. However, recent discoveries of novel plasma markers implicated in pathophysiology of heart failure and technological advances in imaging provide additional biomarkers which are potentially applicable to HFPEF. The evidence base for plasma extra-cellular matrix (ECM) peptides, galectin-3, ST2, GDF-15 and pentraxin-3 is reviewed. Furthermore, the capabilities of novel imaging techniques to assess existing parameters (e.g. left ventricular ejection fraction, systolic & diastolic function, chamber size) and additional derangements of the ECM, myocardial mechanics and ischaemia evaluation are addressed.
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PMID:Novel plasma and imaging biomarkers in heart failure with preserved ejection fraction. 2878 7

We analyzed previously generated stable monocyte-derived cell line carrying mutation JAK2 V617F. Evaluation of the expression of pro- and antifibrotic factors revealed changes in the production of MMPs and their inhibitors, growth factors, galectin-3, and pentraxin 3 in cells carrying mutation JAK2 in comparison with control non-modified cells.
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PMID:Monocytes with Oncogenic Mutation JAK2 V617F as a Tool for Studies of the Pathogenic Mechanisms of Myelofibrosis. 2950 5

Inflammation, apoptosis and extracellular remodeling play significant roles in cardiovascular disease (CVD) underlying the major causes of mortality in renal patients. In 19 pre-dialysis patients, 21 dialysis patients and 20 control subjects, the concentrations of pentraxin-3, galectin-3, MMP-9 and TIMP-1 were determined by ELISA. CVD risk was calculated according to the Framingham risk score algorithm. Pentraxin-3 was increased in renal patients compared to healthy controls (p<0.001). In contrast, galectin-3 was reduced in hemodialysis patients compared to pre-dialysis patients and controls (p<0.001). In addition, MMP-9 and TIMP-1 were elevated in renal patients compared to controls (p<0.01 and p<0.001, respectively). Logistic regression analyses disclosed associations of galectin-3, MMP-9, pentraxin-3 and glomerular filtration with calculated CVD risk score. Combined testing of pentraxin-3, galectin-3, MMP-9 and glomerular filtration rate can discriminate renal patients with high and low risk of a coronary event.
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PMID:Association of Pentraxin-3, Galectin-3 and Matrix Metalloproteinase-9/Timp-1 with Cardiovascular Risk in Renal Disease Patients. 2959 Jul 22

The aim of the study was to evaluate the ability of following biomarkers as diagnostic tools and risk predictors of AAA: C-reactive protein, interleukin-6, pentraxin-3, galectin-3, procollagen type III N-terminal peptide, C-terminal telopeptide of type I collagen, high-sensitive troponin I, and brain natriuretic peptide. Seventy-two patients with an AAA and 100 healthy individuals were enrolled into the study. We assessed individual biomarker performance and correlation between the AAA diameter and biomarker levels, and also, a multivariate logistic regression was used to design a possible predictive model of AAA growth and rupture risk. We identified following four parameters with the highest potential to find a useful place in AAA diagnostics: galectin-3, pentraxin-3, interleukin-6, and C-terminal telopeptide of type I. The best biomarkers in our evaluation (galectin-3 and pentraxin-3) were AAA diameter-independent. With the high AUC and AAA diameter correlation, the high-sensitive troponin I can be used as an independent prognostic biomarker of the upcoming heart complications in AAA patients. Authors recommend to add biomarkers as additional parameters to the current AAA patient management. Main addition value of biomarkers is in the assessment of the AAA with the smaller diameter. Elevated biomarkers can change the treatment decision, which would be done only based on AAA diameter size. The best way how to manage the AAA patients is to create a reliable predictive model of AAA growth and rupture risk. A created multiparameter model gives very promising results with the significantly higher efficiency compared with the use of the individual biomarkers.
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PMID:Blood biomarker panel recommended for personalized prediction, prognosis, and prevention of complications associated with abdominal aortic aneurysm. 3125 18

The acute-phase protein pentraxin-3 (PTX3) is a component of the innate immune system. Inflammation and tissue injury increased PTX3 in the injured liver, and accordingly, circulating PTX3 was induced in patients with chronic liver diseases. In the present study, PTX3 protein was determined in systemic, hepatic, and portal vein plasma of patients with liver cirrhosis to assess a possible association between hepatic PTX3 release and extent of liver injury. However, PTX3 levels were not related to disease severity. Of note, portal PTX3 levels were higher than concentrations in the hepatic vein. PTX3 in the hepatic and portal veins was negatively correlated with factor V, antithrombin 3, and prothrombin time. PTX3 did neither correlate with C-reactive protein nor galectin-3 or resistin, whereby the latter two proteins are associated with hepatic injury. PTX3 levels were not changed in cirrhosis patients with ascites or varices and did not correlate with the hepatic venous pressure gradient. Likewise, serum PTX3 was not correlated with histological steatosis, inflammation, or fibrosis stage in patients with hepatocellular carcinoma (HCC). Moreover, PTX3 was not associated with tumor node metastasis classification in HCC. Above all, PTX3 increased in hepatic, portal, and systemic blood immediately after transjugular intrahepatic portosystemic shunt (TIPS). Higher PTX3 in portal than hepatic vein plasma and further increase after TIPS suggests that the liver eliminates PTX3 from the circulation. In summary, PTX3 is not of diagnostic value in cirrhosis and HCC patients.
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PMID:Pentraxin-3 is not related to disease severity in cirrhosis and hepatocellular carcinoma patients. 3207 18