Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Nov 25;20(5):170-174.
doi: 10.1002/cld.1245. eCollection 2022 Nov.

Role of galectin-3 in the pathogenesis and progression of biliary atresia

Affiliations
Review

Role of galectin-3 in the pathogenesis and progression of biliary atresia

Dor Yoeli et al. Clin Liver Dis (Hoboken). .

Abstract

Content available: Audio Recording.

PubMed Disclaimer

Conflict of interest statement

C.L.M. consults for Albireo.

Figures

FIGURE 1
FIGURE 1
Effects of galectin‐3 on immune cell response to biliary disease. Extracellular galectin‐3 is critical to the activation and function of macrophages and neutrophils, as well as to the recruitment of various inflammatory cells in response to liver and bile duct injury. Intracellular galectin‐3, known to be expressed in cholangiocytes, has antiapoptotic effects. Figure was created with BioRender.com. All rights and ownership of BioRender content are reserved by BioRender. BioRender content included in the completed graphic is not licensed for any commercial uses beyond publication in a journal.
FIGURE 2
FIGURE 2
Role of galectin‐3 in liver fibrosis in cholestatic disease. Galectin‐3 is crucial to the activation of HSCs into a myofibroblast phenotype in response to hepatocyte or cholangiocyte injury. Activated HSCs release collagen and TGF‐β leading to liver fibrosis. Figure was created with BioRender.com. All rights and ownership of BioRender content are reserved by BioRender. BioRender content included in the completed graphic is not licensed for any commercial uses beyond publication in a journal.
FIGURE 3
FIGURE 3
Therapeutic potential of galectin‐3 inhibition in BA. Use of a galectin‐3 inhibitor at time of Kasai HPE could slow the progression of liver fibrosis by decreasing macrophage and HSC activation, as well as overall immune cell infiltration of the liver. Figure was created with BioRender.com. All rights and ownership of BioRender content are reserved by BioRender. BioRender content included in the completed graphic is not licensed for any commercial uses beyond publication in a journal.

Similar articles

Cited by

References

    1. Bezerra JA, Wells RG, Mack CL, Karpen SJ, Hoofnagle JH, Doo E, et al. Biliary atresia: clinical and research challenges for the twenty‐first century. Hepatology. 2018;68:1163–73. - PMC - PubMed
    1. Ortiz‐Perez A, Donnelly B, Temple H, Tiao G, Bansal R, Mohanty SK. Innate immunity and pathogenesis of biliary atresia. Front Immunol. 2020;11:329. - PMC - PubMed
    1. Dumic J, Dabelic S, Flogel M. Galectin‐3: an open‐ended story. Biochim Biophys Acta. 2006;1760:616–35. - PubMed
    1. Honsawek S, Chongsrisawat V, Praianantathavorn K, Theamboonlers A, Poovorawan Y. Elevation of serum galectin‐3 and liver stiffness measured by transient elastography in biliary atresia. Eur J Pediatr Surg. 2011;21:250–4. - PubMed
    1. Volarevic V, Milovanovic M, Ljujic B, Pejnovic N, Arsenijevic N, Nilsson U, et al. Galectin‐3 deficiency prevents concanavalin A‐induced hepatitis in mice. Hepatology. 2012;55:1954–64. - PubMed