# The emerging regulatory roles of non-coding RNA in Ventilator-induced Lung Injury

## TL;DR

This paper reviews how non-coding RNAs contribute to ventilator-induced lung injury and their potential for diagnosis and treatment.

## Contribution

The paper provides a comprehensive review of the emerging roles of microRNAs and long non-coding RNAs in ventilator-induced lung injury.

## Key findings

- Non-coding RNAs modulate inflammatory pathways like TLR, JAK-STAT, and NF-κB during mechanical ventilation.
- ncRNAs have diagnostic and therapeutic potential in mitigating ventilator-induced lung injury.
- Current research highlights the role of ncRNAs in mechanotransduction processes affecting lung compliance and inflammation.

## Abstract

Ventilator-induced lung injury (VILI) is characterized by pathological features such as infiltration of inflammatory cells, increased alveolar permeability, and changes in lung compliance. The underlying mechanisms responsible for these manifestations during mechanical ventilation remain unclear. Low tidal volume ventilation and positive end-expiratory pressure (PEEP) can mitigate pulmonary edema and improve lung compliance. However, these strategies do not fully prevent VILI, and mortality remains high. Non-coding RNAs (ncRNAs) are involved in mechanotransduction processes during ventilation by modulating cellular functions through the activation of inflammatory signaling pathways, such as Toll-like receptor (TLR), Janus kinase/signal transducer and activator of transcription (JAK-STAT), and nuclear factor kappa-B (NF-κB). These pathways contribute to the development of VILI and possess notable diagnostic, differential diagnostic, and therapeutic potential. This review offers a comprehensive evaluation of current research on microRNAs and long non-coding RNAs in relevant models of VILI.