Related Experiment Video

Updated: Feb 15, 2026

Complementation of Splicing Activity by a Galectin-3 - U1 snRNP Complex on Beads
08:48

Complementation of Splicing Activity by a Galectin-3 - U1 snRNP Complex on Beads

Published on: December 9, 2020

2.5K

Galectin-3 Activation and Inhibition in Heart Failure and Cardiovascular Disease: An Update

Navin Suthahar1, Wouter C Meijers1, Herman H W Silljé1

  • 1University Medical Center Groningen, University of Groningen, Department of Cardiology, PO Box 30.001, 9700 RB Groningen, the Netherlands.

Theranostics
|January 19, 2018
PubMed

Insights

Galectin-3, a key protein in disease, undergoes activation through self-interaction, altering its function. Understanding this activation mechanism is crucial for targeting galectin-3 in various pathologies like fibrosis and heart failure.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pathophysiology

Background:

  • Galectin-3 is a protein involved in numerous physiological and pathophysiological processes.
  • Its expression is altered in response to tissue injury and stress, and it's linked to diseases such as fibrosis, heart failure, atherosclerosis, and diabetes mellitus.
  • Galectin-3 is recognized as a potential therapeutic target due to its role in disease.

Purpose of the Study:

  • To review and synthesize recent literature on galectin-3 activation.
  • To provide novel insights into the mechanisms of galectin-3 activation from a binding perspective.
  • To elucidate how galectin-3 activation is regulated in pathophysiological conditions.

Main Methods:

  • Literature review focusing on galectin-3 binding properties and self-interactions.
  • Analysis of existing data on galectin-3 activation mechanisms.
  • Synthesis of information regarding the regulation of galectin-3 activity in disease contexts.

Main Results:

  • Monomeric extracellular galectin-3 can be activated, broadening its biological activities by modifying carbohydrate-binding properties.
  • Self-interactions of galectin-3 are critical for regulating its extracellular functions.
  • The precise mechanisms of galectin-3 self-interaction and activation remain incompletely understood but are central to its pathophysiological roles.

Conclusions:

  • Galectin-3 activation, particularly through self-interaction, significantly impacts its biological functions.
  • A deeper understanding of galectin-3 binding and activation mechanisms is essential for developing targeted therapies.
  • Further research into galectin-3 regulation in disease states is warranted to explore its therapeutic potential.
Keywords:
Galectin-3carbohydrate binding domaincardiovascular diseasecell-cell adhesionextracellular matrixfibrosisheart failureinteractionrenal disease

More Related Videos

In Silico Clinical Trials for Cardiovascular Disease09:09

In Silico Clinical Trials for Cardiovascular Disease

Published on: May 27, 2022

2.3K
Tachycardia-Induced Cardiomyopathy As a Chronic Heart Failure Model in Swine10:08

Tachycardia-Induced Cardiomyopathy As a Chronic Heart Failure Model in Swine

Published on: February 17, 2018

14.0K

Related Concept Videos

Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
1.0K
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
4.0K
Heart Failure I: Introduction01:27

Heart Failure I: Introduction

Heart failure refers to a clinical syndrome caused by structural or functional cardiac disorders that prevent the heart from pumping an adequate amount of blood to meet the body's metabolic needs. This condition often arises from myocardial infarction or ischemia, leading to decreased cardiac output, reduced tissue perfusion, impaired gas exchange, fluid volume imbalance, and decreased functional ability.Heart failure can result from disruptions in the mechanisms that regulate cardiac output...
966
Psychoneuroimmunology: Cardiovascular Disease01:27

Psychoneuroimmunology: Cardiovascular Disease

Psychoneuroimmunology (PNI) is a multidisciplinary field that examines how psychological factors, particularly stress, interact with the immune system and impact physical health. Research in PNI has shown that chronic or traumatic stress can disrupt both the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. These disruptions contribute to serious health conditions, including cardiovascular diseases.
A key area of focus in PNI is the relationship between stress and coronary...
588
Heart Failure VI: Adjunct Therapies01:22

Heart Failure VI: Adjunct Therapies

Additional therapies for treating patients with heart failure (HF) may include procedural interventions, supplemental oxygen, the management of sleep disorders, and nutritional therapy.Procedural InterventionsImplantable Cardioverter-Defibrillator: For patients at risk of life-threatening arrhythmias due to severe left ventricular dysfunction, an Implantable Cardioverter-Defibrillator (ICD) can detect and terminate these arrhythmias, preventing sudden cardiac death and improving survival rates.
402
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
1.0K