Publications

The goal of this study was to evaluate the ability of Gal‐3 depletion apheresis using an adsorption column with immobilized anti‐Gal‐3‐antibody to reduce inflammation induced by Complete Freund’s Adjuvant injection in a skin inflammation porcine model. Here, we report that plasma perfusion by apheresis through a Gal‐3 binding immuno‐affinity column reduces plasma Gal‐3 levels to below limits of quantitative detection, and results in significant decrease in skin inflammation, including degree and duration of inflammatory lesions. Human plasma was tested ex vivo and found to be efficiently depleted using the anti‐Gal‐3 affinity column. This study demonstrates the potential of Gal‐3 depletion apheresis as a therapeutic method for inflammation‐mediated disease, supporting continued research in this area for clinical application.

The goal of this study was to evaluate the ability of Gal‐3 depletion apheresis using an adsorption column with immobilized anti‐Gal‐3‐antibody to reduce inflammation induced by Complete Freund’s Adjuvant injection in a skin inflammation porcine model. Here, we report that plasma perfusion by apheresis through a Gal‐3 binding immuno‐affinity column reduces plasma Gal‐3 levels to below limits of quantitative detection, and results in significant decrease in skin inflammation, including degree and duration of inflammatory lesions.

This translational study in Critical Care links galectin-3 to septic acute kidney injury (S-AKI): higher serum galectin-3 at ICU admission predicted later AKI and ICU death in adults with sepsis.

In a rat sepsis model (cecum ligation and puncture), pretreatment with modified citrus pectin—a galectin-3 blocker—was associated with lower galactin-3 and IL‑6 levels, fewer cases of AKI, and improved 7‑day survival, supporting galectin-3 as a possible disease pathway and therapeutic target.

Galectin-3 is good diagnostic biomarker of AKI in the patients undergoing cardiac surgery.

Galectin-3 increased immediately after ischemic/reperfusion, as early as 0.5 h after reperfusion.

Pharmacologic inhibition of Gal-3 by MCP attenuated renal dysfunction, renal tubular injury, renal apoptosis, and IL-6 release.

This Frontiers in Physiology review links galectin-3 to acute kidney injury (AKI) and chronic kidney disease (CKD): the lectin’s pro-inflammatory and pro-fibrotic actions are implicated in both conditions, and higher serum galectin-3 is associated with AKI in critically ill patients and with CKD progression and worse outcomes. Across clinical cohorts and animal models—including ischemia-reperfusion, sepsis, hypertensive nephropathy, and renal fibrosis—inhibiting galectin-3 (e.g., with modified citrus pectin) is associated with less kidney injury, inflammation, and fibrosis and, in some settings, lower mortality. The authors argue that galectin-3 may serve as both a biomarker and a therapeutic target in AKI and CKD.