Novel Therapeutic Targets of Endothelial Inflammation in Acute Lung Injury and Acute Respiratory Distress Syndrome

Abstract

Lung microvascular endothelial inflammation and barrier dysfunction play critical roles in the pathogenesis of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Despite recent scientific advances, the mortality of ALI/ARDS is still extremely high because the molecular mechanisms involved in ALI/ARDS remain unclear. In a recent issue of the journal Advanced Science, Baoyinna and colleagues reported that deubiquitinase USP30 induces lung microvascular inflammation and endothelial barrier disruption through the S-adenosylmethionine (SAM) cycle, DNA methylation, and miR-30a-5p down-regulation in ALI/ARDS. Their findings provide a strong rationale for targeting microRNAs, S-adenosylmethionine, DNA methylation, and deubiquitinating enzymes as potential therapeutic strategies for the treatment of ALI/ARDS.

Keywords

Lung / Endothelium / Inflammation / Barrier function / Acute lung injury / Acute respiratory distress syndrome

Ethics Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

Not applicable.

Funding

This work was supported, in whole or in part, by NIH grants HL134934 and HL158909 to Y.S., and by the Department of Veterans Affairs BX005350 to Y.S.

Declaration of Competing Interest

The author declares that he has no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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