Encapsulating taurine into liposomes: A promising therapeutic for liver fibrosis
- PMID: 39534415
- PMCID: PMC11551675
- DOI: 10.3748/wjg.v30.i41.4509
Encapsulating taurine into liposomes: A promising therapeutic for liver fibrosis
Abstract
We summarize the mechanism by which taurine (Tau) inhibits autophagy and induces iron apoptosis in hepatic stellate cells. Tau interacts with autophagy regulates multifunctional proteins, microtubule-associated protein 1 light chain 3 Beta, and autophagy-related gene 5 to inhibit autophagy, binds to ferritin heavy chain 1 and nuclear receptor coactivator 4 to trigger ferritin autophagy, and interacts with glutathione peroxidase 4 to promote iron apoptosis. There is a solid rationale for developing Tau-based therapies targeting autophagy and ferroptosis regulation. From a pharmaceutical point of view, there are certain requirements for Tau protein delivery systems, such as loading efficiency, stability, and targeting. Nanomaterials should also contain a hydrophilic motif similar to Tau to optimize loading efficiency. Since Tau is a hydrophilic molecule with high water solubility, liposomes, micelles, and amphiphilic polymer nanoparticles may represent a superior choice. The nanostructure of the liposome includes a water region and a lipid membrane to sequester hydrophilic and hydrophobic drugs, respectively, whereas Tau is expected to be loaded into the water region. In addition, a representative method of actively targeting hematopoietic stem cells is introduced. A Tau-based method for the treatment of liver fibrosis is proposed based on the formulation of common liposomes (lecithin plus cholesterol).
Keywords: Hepatic stellate cells; Liposome; Liver fibrosis; Nanoparticle delivery systems; Targeted therapy; Taurin.
©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
Conflict of interest statement
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
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