For more than 30 years, Isaac Eliaz, MD, MS, LAc, has investigated, studied, and researched one molecule that continues to appear across seemingly different areas of medicine and disease: Galectin-3.
At the center of this critically important work is a deceptively simple biological question:
What happens when a mechanism designed to help the body survive becomes part of the problem?
The body’s biological survival response is innate and rapid by design. In the face of infection, injury, toxins, or other stressors, autonomic, biochemical, and immune pathways activate quickly to protect the organism. However, the downside of this adaptive response is what I term—the “survival paradox”: protective mechanisms that become persistently activated can contribute to chronic inflammation, immune dysfunction, tissue injury, and eventually, acute and chronic disease. This process is driven by the culprit biomarker, Galectin-3.
Galectin-3 (Gal-3) is a protein that our body naturally produces, and has key roles on an intracellular level. However, a substantial and growing body of research places Gal-3 at the center of multiple inflammatory and immune pathways, implicating it as an important mediator of systemic inflammation, immune dysregulation, and organ dysfunction. Produced in response to stress, illness, injury, toxins, and normal aging, this carbohydrate-binding protein is involved in numerous cellular and extracellular processes that regulate immune signaling, cell adhesion, tissue remodeling, inflammation, fibrosis, and interactions with a wide variety of ligands driving pathogenic impacts at the cellular and tissue levels.
Gal-3’s complex and broad biological reach is the reason I have continued following this molecule for decades—rather than viewing it through the lens of any single disease.
Can Galectin-3 Be Inhibited?
As our understanding of Galectin-3 expands, the clinically relevant question points to a novel—and essential—therapeutic pathway: If excessive or dysregulated Gal-3 activity is involved in disease progression, can that activity be inhibited or modulated to improve outcomes?
This is what led to the development of Modified Citrus Pectin (MCP) over 30 years ago. Today, MCP is one of the most-researched Galectin-3 inhibitors backed by over 100 publications examining its biological and clinical applications.
Unlike unmodified dietary pectin, properly produced MCP has a reduced molecular size and specific structure that allows it to enter the circulation and bind with the carbohydrate-recognition end terminal of the Gal-3 molecule—thereby interfering with pathogenic aspects of excess Gal-3 activity.
Over the last three decades, research on MCP expanded across multiple indications, including inflammation and fibrosis, cardiovascular, liver, and kidney health, neurodegenerative conditions, oncology-related applications, detoxification, immune health, and other areas. From this body of data, MCP stands out as a single ingredient with a broad range of therapeutic applications attributed to its ability to downregulate Galectin-3 activity, along with secondary benefits that include heavy metal chelation properties and prebiotic effects.
Following Galectin-3 Across Disease Pathways
Today, there are more than 10,000 publications on Galectin-3, highlighting its role in complex biological pathways extending beyond chronic inflammatory disease.
Research has linked Gal-3 with both acute and chronic conditions. One of its most important characteristics is that Gal-3 does not operate in isolation. It interacts with macrophages, fibroblasts, extracellular matrix proteins, immune receptors, and numerous cell-surface ligands. In inflammatory and fibrotic processes, it participates across the continuum from early immune activation to prolonged inflammation and tissue fibrosis.
In cancer biology, Gal-3 has been studied for its relationships with proliferation, apoptosis resistance, migration and invasion, angiogenesis, and immune surveillance within the tumor microenvironment. In fact, it plays such a central role in cancer that researchers have termed it, “The Guardian of the Tumor Microenvironment”.
However, it was the growing connection between Gal-3 and acute critical illness that would eventually lead me to investigate its role in critical care.
The Galectin-3–Sepsis Connection
Sepsis presents a fundamentally different clinical challenge from chronic disease.
In chronic illness, there may be time to influence inflammatory signaling over weeks or months. In sepsis and related acute conditions, biological deterioration and multiple organ damage can occur within hours.
For doctors and ICU staff, the challenge far exceeds answering the question, “Can Ga-3 activity be inhibited?”. Rather, my team and I at Eliaz Therapeutics began exploring another possibility: Could circulating Gal-3 be selectively targeted and removed rapidly enough to alter the course of an acute inflammatory cascade as deadly as sepsis?
Our insight gained support from research linking elevated Galectin-3 with sepsis, acute kidney injury, and poor outcomes in critically ill patients.
One multicenter prospective cohort evaluated over 2,000 ICU patients and examined Gal-3 levels at admission in relation to major adverse kidney events and mortality. Elevated Galectin-3 was associated with worse kidney outcomes and death following ICU admission.
Additional research demonstrated how increasing Gal-3 levels, alongside worsening stages of acute kidney injury, are associated with greater mortality.
These findings do not necessarily establish that Gal-3 alone causes sepsis or organ failure. But collectively, they support a growing body of evidence suggesting that Gal-3 may be more than a novel biomarker. An expanding body of literature strongly suggests that Gal-3 instigates and further drives the inflammatory, vascular, and fibrotic processes that contribute to critical illness.
This opened the door to advancing the next phase of Gal-3 management: therapeutic apheresis.
From Galectin-3 Inhibition to Galectin-3 Removal
Therapeutic apheresis is an extracorporeal blood filtration treatment that allows for the removal of selected inflammatory compounds and lipid-soluble toxins from the bloodstream or plasma, while returning the remaining components to the patient. Depending on the type of apheresis, treatment may involve highly selective adsorption of specific targets or broader approaches such as plasma exchange.
This is where fact vs. fiction matters and why it is important to clarify misconceptions of how and when to use different types of apheresis for what kinds of patients, and when treatments are beneficial vs. being potentially harmful. As interest in plasma exchange and selective therapeutic apheresis continues to grow, these distinctions become increasingly critical for healthcare practitioners.
Historically, blood purification has often meant removing broad categories of circulating compounds. The development of treatment-specific devices creates the possibility of targeting individual molecules or defined classes of mediators with greater precision.
Gal-3 offers one example of that evolution.
In my emerging research and clinical work, we have investigated whether selective removal of circulating Gal-3 using highly specialized, selective apheresis filters, could offer a new therapeutic approach for acute inflammatory conditions—including sepsis.9
This possibility is particularly important because, although modern sepsis care includes antibiotics, source control, hemodynamic support, and organ-supportive therapies, there remains a major unmet need for targeted treatments that directly address the dysregulated host response driving organ injury.
What Could the Future of Apheresis Look Like?
The larger question raised by these research developments is not whether every inflammatory disease or aging process should be treated with apheresis. The question that we are exploring through our pioneering work, is whether advances in molecular targeting could make extracorporeal therapies increasingly selective, precise and potentially more effective.
In combination with other leading-edge developments in genomics, diagnostics, and protocol design, our emerging apheresis research points toward the potential for highly targeted, individualized, precision-based treatments designed to intervene in specific biological pathways including dysregulated Gal-3.
In this way, a molecule that participates in normal survival biology may also become an actionable therapeutic target when that same biology becomes dysregulated.
About Dr. Isaac Eliaz, MD, MS, LAc
Isaac Eliaz, MD, MS, LAc, is a physician-scientist and clinician whose work spans laboratory research, clinical practice, integrative medicine, and therapeutic apheresis. His published research has examined Galectin-3 in relation to inflammation, cancer, sepsis, acute kidney injury, and extracorporeal therapies. His work has received NIH-funded research and more recently, Eliaz Therapeutics has received FDA Breakthrough Device Designation for its investigational device designed to selectively remove Gal-3 through apheresis for the treatment of sepsis.
Dr. Eliaz’s career and private practice have followed this science across chronic inflammation, fibrosis, cancer, kidney injury, immune dysregulation, and, more recently, critical illness and sepsis. His pioneering research has helped shape two distinctive therapeutic approaches: first, inhibiting Galectin-3 activity with Modified Citrus Pectin; and later, developing a way to selectively remove Galectin-3 from the bloodstream through therapeutic apheresis.
Learn more at www.dreliaz.org.
References:
- Bouffette S, Botez I, De Ceuninck F. Targeting galectin-3 in inflammatory and fibrotic diseases. Trends Pharmacol Sci. 2023 Aug;44(8):519-531. doi: 10.1016/j.tips.2023.06.001. Epub 2023 Jun 28. PMID: 37391294.
- Boutin L, et al. Elevated plasma Galectin-3 is associated with major adverse kidney events and death after ICU admission. Crit Care. 2022 Jan 6;26(1):13. doi: 10.1186/s13054-021-03878-x. PMID: 34991653; PMCID: PMC8740042.
- Brzački V, et al. Circulating and Tissue Galectin-3 in Gastrointestinal Inflammation: Clinical Significance and Biomarker Potential. Cells. 2025 Sep 29;14(19):1521. doi: 10.3390/cells14191521. PMID: 41090750; PMCID: PMC12524185.
- Eliaz I, Raz A. Pleiotropic Effects of Modified Citrus Pectin. Nutrients. 2019 Nov 1;11(11):2619. doi: 10.3390/nu11112619. PMID: 31683865; PMCID: PMC6893732.
- Lurje I, et al. The Role of Galectin-3 in Liver Inflammation and Fibrosis. J Inflamm Res. 2026 Jan 8;19:572637. doi: 10.2147/JIR.S572637. PMID: 41859377; PMCID: PMC12998635.
- Ruvolo PP. Galectin 3 as a guardian of the tumor microenvironment. Biochim Biophys Acta. 2016 Mar;1863(3):427-437. doi: 10.1016/j.bbamcr.2015.08.008. Epub 2015 Aug 8. PMID: 26264495
- Seropian IM, et al. Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: Implications for heart failure and transplantation. Cytokine Growth Factor Rev. 2024 Dec;80:47-58. doi: 10.1016/j.cytogfr.2024.10.002. Epub 2024 Oct 20. PMID: 39482190.
- Sun H, Jiang H, Eliaz A, Kellum JA, Peng Z, Eliaz I. Galectin-3 in septic acute kidney injury: a translational study. Crit Care. 2021 Mar 18;25:109. doi: 10.1186/s13054-021-03538-0. PMID: 33736691; PMCID: PMC7977587.
- Sun H, Peng J, Cai S, Nie Q, Li T, Kellum JA, Eliaz I, Peng Z. A translational study of Galectin-3 as an early biomarker and potential therapeutic target for ischemic-reperfusion induced acute kidney injury. J Crit Care. 2021 Oct;65:192-199. doi: 10.1016/j.jcrc.2021.06.013. Epub 2021 Jul 2. PMID: 34225083.
- Sun Z, Qu J, Peng S, Hu Y, Eliaz A, Chertow GM, Eliaz I, Peng Z. Therapeutic Galectin-3 Apheresis Improves Sepsis Outcomes Through Coordinated Neutrophil Modulation and Endothelial Barrier Preservation: A Translational Study. MedComm (2020). 2026 Apr;7(4):e70659. doi: 10.1002/mco2.70659. Epub 2026 Mar 15. PMID: 41930343; PMCID: PMC13042957.
- Yu Q, et al. Galectin-3 in sepsis: A multifaceted regulator of innate immunity, vascular dysfunction, and organ injury. Cell Signal. 2026 Sep;145:112613. doi: 10.1016/j.cellsig.2026.112613. Epub 2026 May 25. PMID: 42184932.
