Publications by authors named "Lu-Qi Dai"
Article Synopsis
- - The study examines how mitochondrial damage-related molecules affect lung fluid balance during acute lung injury, utilizing both human patients and gene-altered mice as subjects.
- - Researchers found that exposure to these mitochondrial molecules worsened lung fluid imbalance, while the absence of the formyl peptide receptor-1 gene in mice showed a reduction in this imbalance.
- - Proteomic analysis showed that specific proteins related to ion channels and cell barriers were affected by mitochondrial patterns, leading to decreased stability in rat lung cells via the formyl peptide receptor-1 pathway.
Mitochondrial peptides cause proinflammatory responses in the alveolar epithelium via FPR-1, MAPKs, and AKT: a potential mechanism involved in acute lung injury.
Am J Physiol Lung Cell Mol Physiol
November 2018
Article Synopsis
- Acute lung injury (ALI) leads to lung inflammation and damage to the alveolar epithelium, with mitochondrial damage-associated molecular patterns (DAMPs) like N-formyl peptides (NFPs) playing a significant role in this process.
- In murine models, elevated mitochondrial NADH dehydrogenase 1 and increased formyl peptide receptor (FPR)-1 expression were linked to worse lung injury, while the use of Cyclosporin H (CsH), an FPR1 inhibitor, reduced inflammation.
- The study highlights the involvement of alveolar epithelial cells in the immune response to MTDs during ALI, suggesting a signaling mechanism that includes increased IL-8 production through FPR-1