<abstract xmlns="http://www.w3.org/1999/xhtml"><p> Heart failure is nowadays a common condition associated with high mortality and increased healthcare-related costs. Over the years, the research on heart failure management has been extensive in order to better diagnose and treat the condition. Since the progression of left ventricular dysfunction is a consequence of myocardial inflammation, apopotosis, and fibrosis leading to myocardium remodelling, several molecules that are involved in the inflammation pathways have been explored as possible biomarkers for the condition. The study of biomarkers and their key roles in inflammation could allow early identification of patients with heart failure, improve prognostic assessment, and provide a target for future therapies. Among currently studied biomarkers, extensive research has been conducted on galectin-3, a galactoside-binding lectin, which is synthetised and secreted when cardiomyocytes and fibroblasts are submitted to mechanical stress. Accordingly, it has been hypothesised that galectin-3 could be a promoter of left ventricular dysfunction. Galectin-3 has been shown to mediate inflammation by several different pathways which are further detailed in the current review. Also, we aimed to provide a comprehensive overview of existing evidence on the utility of galectin-3 in clinical settings associated with heart failure.</p></abstract>

Heart failure is nowadays a common condition associated with high mortality and increased healthcare-related costs. Over the years, the research on heart failure management has been extensive in order to better diagnose and treat the condition. Since the progression of left ventricular dysfunction is a consequence of myocardial inflammation, apopotosis, and fibrosis leading to myocardium remodelling, several molecules that are involved in the inflammation pathways have been explored as possible biomarkers for the condition. The study of biomarkers and their key roles in inflammation could allow early identification of patients with heart failure, improve prognostic assessment, and provide a target for future therapies. Among currently studied biomarkers, extensive research has been conducted on galectin-3, a galactoside-binding lectin, which is synthetised and secreted when cardiomyocytes and fibroblasts are submitted to mechanical stress. Accordingly, it has been hypothesised that galectin-3 could be a promoter of left ventricular dysfunction. Galectin-3 has been shown to mediate inflammation by several different pathways which are further detailed in the current review. Also, we aimed to provide a comprehensive overview of existing evidence on the utility of galectin-3 in clinical settings associated with heart failure.

Is galectin-3 a promoter of ventricular dysfunction?

Revista Romana de Medicina de Laborator

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

{"article-title":"Is galectin-3 a promoter of ventricular dysfunction?"}

Heart failure is nowadays a common condition associated with high mortality and increased healthcare-related costs. Over the years, the research on heart...

Is galectin-3 a promoter of ventricular dysfunction?

Publié en ligne: 30 janv. 2018

Pages: 21 - 36

Reçu: 10 sept. 2017

Accepté: 10 déc. 2017

DOI: https://doi.org/10.2478/rrlm-2018-0001

Mots clés
Galectin-3, biomarker, heart failure, dyspnea, ventricular dysfunction, ventricular remodelling

© by Silvia Lupu

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

Is galectin-3 a promoter of ventricular dysfunction?

Publié en ligne: 30 janv. 2018

Pages: 21 - 36

Reçu: 10 sept. 2017

Accepté: 10 déc. 2017

DOI: https://doi.org/10.2478/rrlm-2018-0001

Mots clésGalectin-3, biomarker, heart failure, dyspnea, ventricular dysfunction, ventricular remodelling

© by Silvia Lupu

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

Mots clés
Galectin-3, biomarker, heart failure, dyspnea, ventricular dysfunction, ventricular remodelling