ArticleBMC research notes2015
Molecular network of important genes for systemic sclerosis-related progressive lung fibrosis.
Article in BMC research notes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Linking Antibodies Against Apolipoprotein A-1 to Metabolic Dysfunction-Associated Steatohepatitis in Mice.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundConsiderable progress has been made in illuminating the pathological events for systemic sclerosis (SSc)-related progressive lung fibrosis. The molecular events that lead to SSc-related progressive lung fibrosis need to be defined. Some important genes have been identified from a recent study in humans. We aim to construct and compare the similarities and differences of molecular pathways between SSc-related progressive lung fibrosis and normal lungs of humans and mice.
methodsWe used the analytical approach of association of key genes in SSc-related progressive lung fibrosis. We first identified the probes for genes of SSc-related progressive lung fibrosis and analyzed the pathways in human lung using data generated by microarray. We then analyzed the gene pathways in mouse lung for similar sets of probes. Gene expression data from livers were used to compare with that in lung in both humans and mice.
resultsOur analysis indicated that, in humans, the expression levels of genes for macrophage activation are more strongly associated with each other than that in mice. In both humans and mice, the associations of these genes are much greater in the lung than that in the liver. The association in gene expression between humans and mice are similar for IFN-regulated genes and profibrotic/Tgfβ-regulated genes.
conclusionOur analysis reveals the differences and similarities of the network of key genes between humans and mice during the molecular processes that eventually lead to fibrosis in the lung.
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