FBLN1 regulates ferroptosis in acute respiratory distress syndrome by reducing free ferrous iron by inhibiting the TGF-β/Smad pathway DOI Creative Commons
Yaping Yuan,

Youbo Wang,

Yu-Feng Yan

et al.

PLoS ONE, Journal Year: 2024, Volume and Issue: 19(12), P. e0314750 - e0314750

Published: Dec. 13, 2024

Background Acute respiratory distress syndrome (ARDS) / acute lung injury (ALI) is a serious medical disease characterized by pulmonary dysfunction and inflammation. This study aims to determine the main molecular modules linked ARDS investigate role of Fibulin-1 (FBLN1) in regulating ferroptosis ARDS. Methods Weighted Gene Co-expression Network Analysis (WGCNA) was employed on GSE263867 dataset find key associated with ALI. Differentially expressed genes (DEGs) protein-protein interaction (PPI) networks were analyzed. MLE-12 cells treated lipopolysaccharide (LPS) induce ferroptosis. In vitro studies conducted effects FBLN1 Transforming Growth Factor Beta 1 (TGF-β) overexpression cell viability, oxidative stress markers, ferroptosis-related proteins. Results WGCNA identified turquoise module as significantly negatively correlated Five overlapping ( GRIA1 , OGN COL14A1 COL6A3 ) downregulated samples. LPS treatment induced cells, indicated increased malondialdehyde (MDA), lipid reactive oxygen species (ROS), ferrous iron (Fe 2 ⁺) levels, decreased viability glutathione (GSH) levels. partially reversed these effects. Additionally, inhibited TGF-β/Smad signaling pathway, shown TGF-β p-Smad protein exacerbated LPS-induced ferroptosis, reducing GSH counteracted this effect, suggesting antagonistic roles for Conclusion highlights critical regulator Targeting pathway modulate expression offers potential therapeutic strategy alleviate mitigate inflammatory diseases.

Language: Английский

ASK1 inhibition by selonsertib attenuates elastase-induced emphysema in mice DOI

Priscilla Cristine de Oliveira Mineiro,

Vanderlei da Silva Fraga‐Junior, Aline de Oliveira Pontes Cardoso

et al.

Life Sciences, Journal Year: 2025, Volume and Issue: unknown, P. 123600 - 123600

Published: April 1, 2025

Language: Английский

Citations

0
Glutathione Attenuates Diesel Exhaust-Induced Lung Epithelial Injury via NF-κB/Nrf2/GPX4-Mediated Ferroptosis DOI

Ekta Nagar,

Naresh Singh, Neeru Saini

et al.

Toxicology, Journal Year: 2025, Volume and Issue: unknown, P. 154154 - 154154

Published: April 1, 2025

Language: Английский

Citations

0
Ficolin A knockout alleviates sepsis-induced severe lung injury in mice by restoring gut Akkermansia to inhibit S100A4/STAT3 pathway DOI
Xu Wu,

Weixia Xuan,

Xiaoping Yang

et al.

International Immunopharmacology, Journal Year: 2023, Volume and Issue: 121, P. 110548 - 110548

Published: June 24, 2023

Language: Английский

Citations

8
Hyperoside attenuates sepsis-induced acute lung injury by Nrf2 activation and ferroptosis inhibition DOI

Kuida Chen,

Shipeng Lu, Ke Shi

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 145, P. 113734 - 113734

Published: Dec. 10, 2024

Language: Английский

Citations

2
FBLN1 regulates ferroptosis in acute respiratory distress syndrome by reducing free ferrous iron by inhibiting the TGF-β/Smad pathway DOI Creative Commons
Yaping Yuan,

Youbo Wang,

Yu-Feng Yan

et al.

PLoS ONE, Journal Year: 2024, Volume and Issue: 19(12), P. e0314750 - e0314750

Published: Dec. 13, 2024

Background Acute respiratory distress syndrome (ARDS) / acute lung injury (ALI) is a serious medical disease characterized by pulmonary dysfunction and inflammation. This study aims to determine the main molecular modules linked ARDS investigate role of Fibulin-1 (FBLN1) in regulating ferroptosis ARDS. Methods Weighted Gene Co-expression Network Analysis (WGCNA) was employed on GSE263867 dataset find key associated with ALI. Differentially expressed genes (DEGs) protein-protein interaction (PPI) networks were analyzed. MLE-12 cells treated lipopolysaccharide (LPS) induce ferroptosis. In vitro studies conducted effects FBLN1 Transforming Growth Factor Beta 1 (TGF-β) overexpression cell viability, oxidative stress markers, ferroptosis-related proteins. Results WGCNA identified turquoise module as significantly negatively correlated Five overlapping ( GRIA1 , OGN COL14A1 COL6A3 ) downregulated samples. LPS treatment induced cells, indicated increased malondialdehyde (MDA), lipid reactive oxygen species (ROS), ferrous iron (Fe 2 ⁺) levels, decreased viability glutathione (GSH) levels. partially reversed these effects. Additionally, inhibited TGF-β/Smad signaling pathway, shown TGF-β p-Smad protein exacerbated LPS-induced ferroptosis, reducing GSH counteracted this effect, suggesting antagonistic roles for Conclusion highlights critical regulator Targeting pathway modulate expression offers potential therapeutic strategy alleviate mitigate inflammatory diseases.

Language: Английский

Citations

2