Galectin as Disease Biomarker

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Gene and Cell Therapy".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 1416

Special Issue Editors


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Guest Editor
1. School of Health Sciences and Institute of Biomedicine-iBiMED, University of Aveiro, 3810-193 Aveiro, Portugal
2. Cardiology Department, Centro Hospitalar do Baixo Vouga, 3810-164 Aveiro, Portugal
Interests: heart; galectin; disease biomarker; immunological diseases

Special Issue Information

Dear Colleagues,

Introduction:

Galectins, an integral class of lectins consisting of eleven members in humans, have been the focus of countless scientific efforts due to their profound importance in immunological diseases. Because of their ability to function as potent mediators of immune responses, abnormalities in their expression have been routinely associated with a wide range of immunological diseases. The overwhelming information about these intriguing proteins has generated a great deal of interest in their potential role in pathological conditions, particularly inflammation, fibrosis, and cancer.

Table of Contents:

  • The galectin protein family: an introduction
  • Galectins in humans: an overview of the eleven members
  • Diverse cellular expression and intracellular distribution

Galectins in pathological conditions

  • Role in inflammation
  • Association with fibrosis
  • Impact on cancer pathogenesis

Galectins as potential biomarkers

  • Diagnostic capabilities and prognostic significance
  • Galectins in immunological diseases: trends and associations
  • Recent studies and key findings

Therapeutic potential of galectins

  • Galectins as therapeutic targets: opportunities and challenges
  • Pharmaceutical approaches to treatment: current strategies and future directions
  • Advances in galectin-based therapies: translational perspectives
  • A vision for the future: next steps in galectin research and clinical translation

Editorial Board Comments:

This Special Issue, curated with deep insights and rigorous scientific analysis, seeks to illuminate the multiple roles played by galectins in human health and disease. The wealth of information highlights the compelling need to intensify efforts to develop galectin-based therapeutic approaches to treat numerous human diseases.

Given their importance in disease pathogenesis and progression, galectins undoubtedly represent an exciting area for biomarker research. As the scientific community more deeply explores the intricate dynamics of galectins in pathological contexts, it is critical to translate this burgeoning knowledge into actionable clinical solutions.

With this compilation, we invite researchers, clinicians, and the broader scientific community to delve into the fascinating world of galectins and explore their promising role as crucial diagnostic/prognostic markers as well as avenues for developing transformative therapeutic modalities. The time is indeed ripe to join our collective efforts to unlock the therapeutic potential of these unique proteins.

Prof. Dr. José Mesquita Bastos
Dr. Rui Vitorino
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • galectins
  • disease biomarker
  • lectins
  • immune response mediators
  • immunological diseases
  • diagnostic marker
  • prognostic marker
  • therapeutic target
  • galactose-binding domains
  • cellular expression
  • intracellular distribution
  • pathological states
  • inflammation
  • fibrosis
  • cancer pathogenesis
  • pharmaceutical approaches
  • therapeutic potential
  • clinical translation
  • aberrancies in expression
  • galectin-based therapies

Published Papers (2 papers)

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Research

22 pages, 4731 KiB  
Article
Calpain Small Subunit Mediated Secretion of Galectin-3 Regulates Traction Stress
by Imjoo Jang, Shalini Menon, Indrajyoti Indra, Rabiah Basith and Karen A. Beningo
Biomedicines 2024, 12(6), 1247; https://doi.org/10.3390/biomedicines12061247 - 4 Jun 2024
Viewed by 299
Abstract
The complex regulation of traction forces (TF) produced during cellular migration remains poorly understood. We have previously found that calpain 4 (Capn4), the small non-catalytic subunit of the calpain 1 and 2 proteases, regulates the production of TF independent of the proteolytic activity [...] Read more.
The complex regulation of traction forces (TF) produced during cellular migration remains poorly understood. We have previously found that calpain 4 (Capn4), the small non-catalytic subunit of the calpain 1 and 2 proteases, regulates the production of TF independent of the proteolytic activity of the larger subunits. Capn4 was later found to facilitate tyrosine phosphorylation and secretion of the lectin-binding protein galectin-3 (Gal3). In this study, recombinant Gal3 (rGal3) was added to the media-enhanced TF generated by capn4−/− mouse embryonic fibroblasts (MEFs). Extracellular Gal3 also rescued defects in the distribution, morphology, and adhesive strength of focal adhesions present in capn4−/− MEF cells. Surprisingly, extracellular Gal3 does not influence mechanosensing. c-Abl kinase was found to affect Gal3 secretion and the production of TF through phosphorylation of Y107 on Gal3. Our study also suggests that Gal3-mediated regulation of TF occurs through signaling pathways triggered by β1 integrin but not by focal adhesion kinase (FAK) Y397 autophosphorylation. Our findings provide insights into the signaling mechanism by which Capn4 and secreted Gal3 regulate cell migration through the modulation of TF distinctly independent from a mechanosensing mechanism. Full article
(This article belongs to the Special Issue Galectin as Disease Biomarker)
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12 pages, 630 KiB  
Article
Correlations of sST2 and Gal-3 with Cardiothoracic Ratio in Patients with Chronic Kidney Disease
by Ying-Ju Chen, Che-Yi Chou and Tze-Kiong Er
Biomedicines 2024, 12(4), 791; https://doi.org/10.3390/biomedicines12040791 - 3 Apr 2024
Viewed by 837
Abstract
Chronic kidney disease (CKD) frequently correlates with cardiovascular complications. Soluble suppression of tumorigenicity 2 (sST2) and Galectin-3 (Gal-3) are emerging as cardiac markers with potential relevance in cardiovascular risk prediction. The cardiothoracic ratio (CTR), a metric easily obtainable from chest radiographs, has traditionally [...] Read more.
Chronic kidney disease (CKD) frequently correlates with cardiovascular complications. Soluble suppression of tumorigenicity 2 (sST2) and Galectin-3 (Gal-3) are emerging as cardiac markers with potential relevance in cardiovascular risk prediction. The cardiothoracic ratio (CTR), a metric easily obtainable from chest radiographs, has traditionally been used to assess cardiac size and the potential for cardiomegaly. Understanding the correlation between these cardiac markers and the cardiothoracic ratio (CTR) could provide valuable insights into the cardiovascular prognosis of CKD patients. This study aimed to explore the relationship between sST2, Gal-3, and the CTR in individuals with CKD. Plasma concentrations of sST2 and Gal-3 were assessed in a cohort of 123 CKD patients by enzyme-linked immunosorbent assay (ELISA). On a posterior-to-anterior chest X-ray view, the CTR was determined by comparing the widths of the heart to that of the thorax. The mean concentration of sST2 in the study participants ranged from 775.4 to 4475.6 pg/mL, and the mean concentration of Gal-3 ranged from 4.7 to 9796.0 ng/mL. Significant positive correlations were observed between sST2 and the CTR (r = 0.291, p < 0.001) and between Gal-3 and the CTR (r = 0.230, p < 0.01). Our findings indicate that elevated levels of sST2 and Gal-3 are associated with an increased CTR in CKD patients. This relationship may enable better cardiovascular risk evaluation for CKD patients. Further studies are warranted to explore the clinical implications of these associations. Full article
(This article belongs to the Special Issue Galectin as Disease Biomarker)
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