# Neuronal injury and hepatotoxicity: astrocytes and stellate cells convergence and their role in tissue repair

## TL;DR

This paper explores how astrocytes in the brain and stellate cells in the liver respond to injury and how they might share similar roles in tissue repair.

## Contribution

The paper provides a comparative analysis of the transcriptomes of activated astrocytes and hepatic stellate cells, highlighting potential common therapeutic targets.

## Key findings

- Astrocytes and hepatic stellate cells share glial-related molecules and functional similarities during injury.
- Long non-coding RNAs and microRNAs regulate gene expression in both neuronal and liver injuries.
- Common targets for reducing activation of these cells could lead to new therapeutic strategies.

## Abstract

In the central nervous system, astrocytes are highly specialized non-neuronal cells that are key elements in maintaining neuronal microenvironment homeostasis. These cells provide structural and metabolic support to other brain cells and regulate ion concentrations and the local levels of neurotransmitters such as glutamate. Astrogliosis, characterized by morphological and functional abnormalities, has been implicated in various neuronal disorders. Similarly, hepatic stellate cells drive the initiation and the progression of liver fibrosis. After liver injury, hepatic stellate cells are activated through inflammatory mediators and differentiate into activated myofibroblasts. Hepatic stellate cells express several glial-related molecules, suggesting functional similarities between these two cell types, which paves the way for a better understanding of crucial targets for neuronal and liver repair. We present herein a compressive update of our current knowledge of the transcriptome of activated hepatic stellate cells during liver injury and contrast it with that of reactive astrocytes in neuronal diseases. Furthermore, we summarize the plausible involvement of long non-coding and microRNAs in the transcriptional regulation of specific genes during neuronal and liver injuries. Finally, we discuss possible common targets and novel strategies to diminish the activation of stellate cells and astrocytes as therapeutic strategies. In addition, we highlight new insights into the brain-liver axis.