ArticleNeurogenesis (Austin, Tex.)2016
Peroxisome proliferator-activated receptor γ (PPARγ) activation: A key determinant of neuropathogeny during congenital infection by cytomegalovirus.
Article in Neurogenesis (Austin, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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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2 citing papers in PubMed, 4 citations in OpenAlex.
- Cytomegalovirus infection of the fetal brain: intake of aspirin during pregnancy blunts neurodevelopmental pathogenesis in the offspring.Journal of neuroinflammation · 2024Article
- Neural Stem Cells: What Happens When They Go Viral?Viruses · 2021Review
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Abstract
Congenital infection by human cytomegalovirus (HCMV) might result in permanent neurological sequelae, including sensorineural deafness, cerebral palsies or devastating neurodevelopmental abnormalities. We recently disclosed that Peroxisome Proliferator-Activated Receptor gamma (PPARγ), a transcription factor of the nuclear receptor superfamily, is a key determinant of HCMV pathogenesis in developing brain. Using neural stem cells from human embryonic stem cells, we showed that HCMV infection strongly increases levels and activity of PPARγ in NSCs. Further in vitro experiments showed that PPARγ activity inhibits the neuronogenic differentiation of NSCs into neurons. Consistently, increased PPARγ expression was found in brain section of fetuses infected by HCMV, but not in uninfected controls. In this commentary, we summarize and discuss our findings and the new insights they provide on the neuropathogenesis of HCMV congenital infection.
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