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

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

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.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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