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: Taurin; Liposome; Liver fibrosis; Targeted therapy; Nanoparticle delivery systems; Hepatic stellate cells

Core Tip: Nanoparticle delivery systems are effective for delivering taurine (Tau). The nanoarchitecture of liposomes includes a water zone and a lipid membrane to accommodate hydrophilic and hydrophobic drugs, respectively. Tau is a hydrophilic molecule with high water solubility, and it is expected to be loaded into the water zone. In theory, hepatic stellate cells (HSCs) may be targeted by Tau-incorporated liposomes via two mechanisms: Passive targeting and active targeting. Active targeting is more robust as it takes advantage of the unique features of the lesion site. Based on a formulation for common liposomes (lecithin plus cholesterol), Tau-based therapeutics was proposed to treat liver fibrosis as follows: A targetable liposome was fabricated through the combination of common lecithin and cholesterol, along with modified lecithin or cholesterol with HSC targetability. Tau was dispersed into the water zone of this liposomal system.