The Potential Application of Magnetic Nanoparticles for Liver Fibrosis Theranostics.

Aziz Eftekhari,Rovshan Khalilov,Magali Cucchiarini,Huseyn Abiyev,Allahveirdy Arjmand,Ayyub Asheghvatan,Taras Kavetskyy,Ondrej Šauša,Helena Švajdlenková,Oleh Smutok,Elham Ahmadian

doi:10.3389/fchem.2021.674786

Abstract

Liver fibrosis is a major cause of morbidity and mortality worldwide due to chronic liver damage and leading to cirrhosis, liver cancer, and liver failure. To date, there is no effective and specific therapy for patients with hepatic fibrosis. As a result of their various advantages such as biocompatibility, imaging contrast ability, improved tissue penetration, and superparamagnetic properties, magnetic nanoparticles have a great potential for diagnosis and therapy in various liver diseases including fibrosis. In this review, we focus on the molecular mechanisms and important factors for hepatic fibrosis and on potential magnetic nanoparticles-based therapeutics. New strategies for the diagnosis of liver fibrosis are also discussed, with a summary of the challenges and perspectives in the translational application of magnetic nanoparticles from bench to bedside.

Highlights

The unique intrinsic regenerative properties of the liver have long been known, reaching up to 70% in healthy liver tissue (Michalopoulos and Bhushan, 2021)
The current review summarizes potential targets and the application of emerging Magnetic nanoparticles (MNPs) for theranostic purposes against hepatic fibrosis
During the progression of liver fibrosis, hepatic stellate cell (HSC)-derived ECM fills the empty spaces resulting from the traveling of hepatocytes

Summary

Introduction

The unique intrinsic regenerative properties of the liver have long been known, reaching up to 70% in healthy liver tissue (Michalopoulos and Bhushan, 2021). During the progression of liver fibrosis, hepatic stellate cell (HSC)-derived ECM fills the empty spaces resulting from the traveling of hepatocytes. The inflammatory response could be induced by hepatocyte damage leading to the activation of macrophages and to a production of ROS and TGF-β1 and to the differentiation of quiescent HSCs in MFBs which in turn may trigger liver fibrosis.

Results

Conclusion