AI Article Synopsis
- Acute lung injury (ALI), which can lead to severe respiratory issues, is influenced by factors like lipopolysaccharides (LPS) and involves an important gene called WWOX, known to respond to environmental stress.
- Research shows that LPS reduces WWOX expression and the autophagy marker MAP1LC3B in lung cells, indicating a potential link to ALI development.
- Overexpressing WWOX increases autophagy and mitigates inflammatory responses in ALI models, suggesting it may protect against ALI through its interactions with the mTOR-ULK1 signaling pathway.
Article Abstract
Acute lung injury (ALI) is characterized by acute systemic inflammatory responses that may lead to severe acute respiratory distress syndrome (ARDS). The clinical course of ALI/ARDS is variable; however, it has been reported that lipopolysaccharides (LPS) play a role in its development. The fragile chromosomal site gene WWOX is highly sensitive to genotoxic stress induced by environmental exposure and is an important candidate gene for exposure-related lung disease research. However, the expression of WWOX and its role in LPS-induced ALI still remain unidentified. This study investigated the expression of WWOX in mouse lung and epithelial cells and explored the role of WWOX in LPS-induced ALI model in vitro and in vivo. In addition, we explored one of the possible mechanisms by which WWOX alleviates ALI from the perspective of autophagy. Here, we observed that LPS stimulation reduced the expression of WWOX and the autophagy marker microtubule-associated protein 1 light chain 3β-II (MAP1LC3B/LC3B) in mouse lung epithelial and human epithelial (H292) cells. Overexpression of WWOX led to the activation of autophagy and inhibited inflammatory responses in LPS-induced ALI cells and mouse model. More importantly, we found that WWOX interacts with mechanistic target of rapamycin [serine/threonine kinase] (mTOR) and regulates mTOR and ULK-1 signaling-mediated autophagy. Thus, reduced WWOX levels were associated with LPS-induced ALI. WWOX can activate autophagy in lung epithelial cells and protect against LPS-induced ALI, which is partly related to the mTOR-ULK1 signaling pathway.
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| http://dx.doi.org/10.1016/j.intimp.2022.109671 | DOI Listing |
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Article Synopsis
- Ripk3 is key in acute lung injury (ALI) by driving endothelial cell damage and inflammation, although the exact mechanisms are not fully understood.
- Studies using Ripk3-deficient mice revealed that removing Ripk3 improved lung tissue health, decreased inflammation, oxidative stress, and endothelial dysfunction after exposure to lipopolysaccharide (LPS).
- Ripk3 was found to inhibit the AMPK pathway and promote necroptosis in endothelial cells by affecting mitochondrial function, suggesting it could be a target for new treatments for ALI.
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