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Review
. 2023 Jan 11;12(2):604.
doi: 10.3390/jcm12020604.

Long Noncoding RNA: A Novel Insight into the Pathogenesis of Acute Lung Injury

Affiliations
Review

Long Noncoding RNA: A Novel Insight into the Pathogenesis of Acute Lung Injury

Saugata Dutta et al. J Clin Med. .

Abstract

Acute lung injury (ALI) and its severe form, acute respiratory distress syndrome (ARDS), represent an acute stage of lung inflammation where the alveolar epithelium loses its functionality. ALI has a devastating impact on the population as it not only has a high rate of incidence, but also has high rates of morbidity and mortality. Due to the involvement of multiple factors, the pathogenesis of ALI is complex and is not fully understood yet. Long noncoding RNAs (lncRNAs) are a group of non-protein-coding transcripts longer than 200 nucleotides. Growing evidence has shown that lncRNAs have a decisive role in the pathogenesis of ALI. LncRNAs can either promote or hinder the development of ALI in various cell types in the lungs. Mechanistically, current studies have found that lncRNAs play crucial roles in the pathogenesis of ALI via the regulation of small RNAs (e.g., microRNAs) or downstream proteins. Undoubtedly, lncRNAs not only have the potential to reveal the underlying mechanisms of ALI pathogenesis but also serve as diagnostic and therapeutic targets for the therapy of ALI.

Keywords: acute respiratory distress syndrome; inflammation; noncoding RNA; pulmonary disease.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
LncRNA mechanisms of action. (A) LncRNA is working as a guide molecule to guide protein recruitment to its desired location to facilitate epigenetic modification. (B) LncRNA is working as a scaffold to provide the proteins with a structural framework. (C) LncRNA is working as a signal molecule (without any protein) to regulate the transcription of downstream genes. (D) LncRNA is working as a signal molecule (along with a protein) to regulate the transcription of downstream genes. (E) LncRNA is working as a decoy (for a DNA molecule) to regulate the transcription of downstream genes. (F) LncRNA is working as a decoy (for an RNA molecule) to regulate the transcription of downstream genes.

References

    1. Nanchal R.S., Truwit J.D. Recent advances in understanding and treating acute respiratory distress syndrome. F1000Research. 2018;7:1322. doi: 10.12688/f1000research.15493.1. - DOI - PMC - PubMed
    1. Parekh D., Dancer R.C., Thickett D.R. Acute lung injury. Clin. Med. 2011;11:615–618. doi: 10.7861/clinmedicine.11-6-615. - DOI - PMC - PubMed
    1. Johnson E.R., Matthay M.A. Acute Lung Injury: Epidemiology, Pathogenesis, and Treatment. J. Aerosol Med. Pulm. Drug Deliv. 2010;23:243–252. doi: 10.1089/jamp.2009.0775. - DOI - PMC - PubMed
    1. Luce J.M. Acute lung injury and the acute respiratory distress syndrome. Crit. Care Med. 1998;26:369–376. doi: 10.1097/00003246-199802000-00043. - DOI - PubMed
    1. Raghavendran K., Pryhuber G., Chess P., Davidson B., Knight P., Notter R. Pharmacotherapy of Acute Lung Injury and Acute Respiratory Distress Syndrome. Curr. Med. Chem. 2008;15:1911–1924. doi: 10.2174/092986708785132942. - DOI - PMC - PubMed

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