ArticleFEBS open bio2020
Knockout of cytochrome P450 1A1 enhances lipopolysaccharide-induced acute lung injury in mice by targeting NF-κB activation.
Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Excessive activation of JAK-STAT signaling contributes to inflammation induced by acuteVirulence · 2025Article
- Cytochrome P450 (CYP) 1 enzymes in acute lung injury: from molecular insights to therapeutic implications.Redox report : communications in free radical research · 2025Review
- Epigenetic mechanisms mediate cytochrome P450 1A1 expression and lung endothelial injury caused by MRSA in vitro and in vivo.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Endothelial cell dynamics in sepsis-induced acute lung injury and acute respiratory distress syndrome: pathogenesis and therapeutic implications.Cell communication and signaling : CCS · 2024Review
- Elevated expression of TNFRSF4 impacts immune cell infiltration and gene mutation in hepatocellular carcinoma.Cancer biomarkers : section A of Disease markers · 2023Article
- The protective effect of natural medicines against excessive inflammation and oxidative stress in acute lung injury by regulating the Nrf2 signaling pathway.Frontiers in pharmacology · 2022Review
- A dual immune signature of CD8+ T cells and MMP9 improves the survival of patients with hepatocellular carcinoma.Bioscience reports · 2021Article
- Anti-TWEAK Antibody Alleviates Renal Interstitial Fibrosis by Increasing PGC-1α Expression in Lupus Nephritis.Journal of inflammation research · 2021Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI) is accompanied by overactivation of multiple pro-inflammatory factors. Cytochrome P450 1A1 (CYP1A1) has been shown to aggravate lung injury in response to hyperoxia. However, the relationship between CYP1A1 and lipopolysaccharide (LPS)-induced ALI is unknown. In this study, CYP1A1 was shown to be upregulated in mouse lung in response to LPS. Using CYP1A1-deficient (CYP1A1-/-) mice, we found that CYP1A1 knockout enhanced LPS-induced ALI, as evidenced by increased TNF-α, IL-1β, IL-6, and nitric oxide in lung; these effects were mediated by overactivation of NF-κB and iNOS. Furthermore, we found that aspartate aminotransferase, lactate dehydrogenase, creatine kinase, and creatinine levels were elevated in serum of LPS-induced CYP1A1-/- mice. Altogether, these data provide novel insights into the involvement of CYP1A1 in LPS-induced lung injury.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.