# Silencing epileptic storms: targeting miRNA-lncRNA crosstalk in astrocytes and microglia to disarm neuroinflammatory triggers

## TL;DR

This paper explores how microRNAs and long noncoding RNAs interact in glial cells to drive epilepsy-related inflammation, offering new targets for treatment.

## Contribution

It is the first to systematically explain the combined role of miRNAs and lncRNAs in epilepsy through glial cell processes.

## Key findings

- miRNAs regulate astrocyte and microglia phenotype and inflammation in epilepsy.
- lncRNAs act as competitive endogenous RNAs to modulate miRNA function.
- The miRNA-lncRNA crosstalk influences glial cell polarization and transcellular communication.

## Abstract

Epilepsy is a chronic neurological disorder characterized by abnormal synchronous discharges of neurons in the brain. It affects approximately 70 million people worldwide, and approximately 30% of patients are resistant to existing antiepileptic drugs. Repeated seizures can lead to neuronal damage, glial cell activation and neuroinflammation, creating a vicious cycle of seizures, inflammation, and neuronal damage. Recent studies have shown that microRNAs play a key role in the pathological process of epilepsy by regulating the phenotype, inflammatory response and metabolic function of astrocytes and microglia. In addition, long noncoding RNAs, as upstream regulators of miRNAs, influence miRNA function by acting as competitive endogenous RNAs, further regulating glial cell activation and inflammatory responses. This paper is the first to systematically elucidate the synergistic role of miRNAs and lncRNAs in epilepsy through glial cell polarization, metabolic imbalance and exosome-mediated transcellular communication, providing a theoretical framework for the development of multitargeted intervention strategies.