Galectins are a family of proteins, which preferentially bind to B-galactoside residues on a variety of molecules. Members of this family have been shown to play functional roles in inflammation and autoimmune pathologies, where they act at key stages of the inflammatory response, including mast cell degranulation, apoptosis and platelet activation. They also modulate (both positively and negatively) leukocyte trafficking into tissue and clearance of the inflammatory infiltrate. Increased serum levels of galectins in inflammatory pathologies such as rheumatoid arthritis and diabetes have been reported and may indicate potential roles as biomarkers of pathology.
The immunoregulatory functions of galectins are complex with actions reported intracellularly as well as through interactions with cell surface receptors. New evidence also supports roles for galectins through interaction with inflammatory mediators such as chemokines thus increasing the complexity of galectin biology during inflammation. As a result of the significant involvement of galectins in many physiological functions and pathologies, there is increasing attention as its role as a potential pharmacological target.
For example, studies have shown a strong link between galectins and autoimmune pathologies, and modulation of galectin expression in response to inflammatory mediators is widely reported. Recently a link has been identified between aging and galectin expression and function in the context of autoimmune disease. Aging is associated with a chronic low-grade inflammation and further studies are required to understand galectin biology in this context as well as in more advanced models of chronic inflammation and associated co-morbidities. Translating our understanding to a pharmacological perspective, studies have already shown that the administration of Galectin-1 can inhibit acute inflammation.
In order to facilitate the advancements of this potential, the goal of this current Research Topic is to invite researchers to contribute reviews and primary research articles on novel galectin pharmacology in the context of inflammatory disease, and how this can pave way for future potential drug treatments. Many advances have been made in the galectin field, yet the molecular and cellular mechanisms involved in galectin function remain poorly defined. Studies to date have largely focused on utilizing recombinant galectins to study function or global knockout mice. The time is right to extend these studies to conditional, tissue specific knockouts.
We welcome the below sub-topic themes, but not limited to:
• Insights into the cellular and molecular mechanisms involved in galectin production, release and function and its implication for novel therapeutic approaches
• Understanding the role of galectins in disease (inflammatory and autoimmune)
• Therapeutic targeting of galectins- success and challenges
• Galectins as biomarkers of inflammatory pathologies
Topic Editor Asif Iqbal currently receives funding from F. Hoffmann-La Roche. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
Galectins are a family of proteins, which preferentially bind to B-galactoside residues on a variety of molecules. Members of this family have been shown to play functional roles in inflammation and autoimmune pathologies, where they act at key stages of the inflammatory response, including mast cell degranulation, apoptosis and platelet activation. They also modulate (both positively and negatively) leukocyte trafficking into tissue and clearance of the inflammatory infiltrate. Increased serum levels of galectins in inflammatory pathologies such as rheumatoid arthritis and diabetes have been reported and may indicate potential roles as biomarkers of pathology.
The immunoregulatory functions of galectins are complex with actions reported intracellularly as well as through interactions with cell surface receptors. New evidence also supports roles for galectins through interaction with inflammatory mediators such as chemokines thus increasing the complexity of galectin biology during inflammation. As a result of the significant involvement of galectins in many physiological functions and pathologies, there is increasing attention as its role as a potential pharmacological target.
For example, studies have shown a strong link between galectins and autoimmune pathologies, and modulation of galectin expression in response to inflammatory mediators is widely reported. Recently a link has been identified between aging and galectin expression and function in the context of autoimmune disease. Aging is associated with a chronic low-grade inflammation and further studies are required to understand galectin biology in this context as well as in more advanced models of chronic inflammation and associated co-morbidities. Translating our understanding to a pharmacological perspective, studies have already shown that the administration of Galectin-1 can inhibit acute inflammation.
In order to facilitate the advancements of this potential, the goal of this current Research Topic is to invite researchers to contribute reviews and primary research articles on novel galectin pharmacology in the context of inflammatory disease, and how this can pave way for future potential drug treatments. Many advances have been made in the galectin field, yet the molecular and cellular mechanisms involved in galectin function remain poorly defined. Studies to date have largely focused on utilizing recombinant galectins to study function or global knockout mice. The time is right to extend these studies to conditional, tissue specific knockouts.
We welcome the below sub-topic themes, but not limited to:
• Insights into the cellular and molecular mechanisms involved in galectin production, release and function and its implication for novel therapeutic approaches
• Understanding the role of galectins in disease (inflammatory and autoimmune)
• Therapeutic targeting of galectins- success and challenges
• Galectins as biomarkers of inflammatory pathologies
Topic Editor Asif Iqbal currently receives funding from F. Hoffmann-La Roche. The other Topic Editors declare no competing interests with regard to the Research Topic subject.