Understanding Galectin-3's Role in Diastolic Dysfunction: A Contemporary Perspective

Abstract

Diastolic dysfunction, a prevalent condition characterized by impaired relaxation and filling of the left ventricle, significantly contributes to heart failure with preserved ejection fraction (HFpEF). Galectin-3, a β-galactoside-binding lectin, has garnered attention as a potential biomarker and mediator of fibrosis and inflammation in cardiovascular diseases. This comprehensive review investigates the impact of galectin-3 on diastolic dysfunction. We explore its molecular mechanisms, including its involvement in cellular signaling pathways and interaction with components of the extracellular matrix. Evidence from both animal models and clinical studies elucidates galectin-3's role in cardiac remodeling, inflammation, and fibrosis, shedding light on the underlying pathophysiology of diastolic dysfunction. Additionally, we examine the diagnostic and therapeutic implications of galectin-3 in diastolic dysfunction, emphasizing its potential as both a biomarker and a therapeutic target. This review underscores the significance of comprehending galectin-3's role in diastolic dysfunction and its promise in enhancing diagnosis and treatment approaches for HFpEF patients.

Keywords: biomarker; cardiac remodeling; diastolic dysfunction; fibrosis; galectin-3; heart failure.

Figure 1

Cellular signaling pathways of galectin-3 in cardiac diastolic pathophysiology.

Figure 2

The pathophysiology of galectin-3 interacted with extracellular matrix components in cardiac diastolic dysfunction.

Figure 3

The role of galectin-3 in inflammation, fibrosis, and heart remodeling leading to cardiac diastolic dysfunction.