ArticleJCI insight2025
Multiomics analysis unveils an inosine-sensitive DNA damage response in neurogenic bladder after spinal cord injury.
Article in JCI insight, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Integrated transcriptomic and proteomic analyses identify novel biomarkers of bladder outlet obstruction.bioRxiv : the preprint server for biology · 2026Article
- Methodological Landscape of DNA Damage Response Detection: From Conventional Assays to Future Innovations.Current issues in molecular biology · 2026Review
- Intravesical instillation of pirfenidone/polydopamine nanoparticles for managing neurogenic bladder post-spinal cord injury by alleviating bladder inflammation and fibrosis.Journal of nanobiotechnology · 2026Article
- Microbial dysbiosis and predictive neuroactive functional profiles in paediatric neurogenic bladder: an exploratory machine learning-based approach.Frontiers in cellular and infection microbiology · 2026Article
- Machine Learning Identifies FLNA as a Key Molecular Target Regulating Neuronal Apoptosis after Spinal Cord Injury.Journal of molecular neuroscience : MN · 2025Article
Corrections and comments
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Authors and funding
22 authors.
Funding
Abstract
Spinal cord injury (SCI) evokes profound dysfunction in hollow organs such as the urinary bladder and gut. Current treatments are limited by a lack of molecular data to inform novel therapeutic avenues. Previously, we showed that systemic treatment with the neuroprotective agent inosine improved bladder function following SCI in rats. Here, we applied integrated multi-omics analysis to explore molecular alterations in the bladder over time and their sensitivity to inosine following SCI. Canonical signaling pathways regulated by SCI included those associated with protein synthesis, neuroplasticity, wound healing, and neurotransmitter degradation. Upstream regulator and causal network analysis predicted multiple effectors of DNA damage response signaling following injury, including poly-ADP ribose phosphorylase-1 (PARP1). Markers of DNA damage (γH2AX, ATM/ATR substrates) and PARP activity were increased in bladder tissue following SCI and attenuated with inosine treatment. Inosine treatment also attenuated oxidative DNA damage in rat bladder cells in vitro. Proteomics analysis suggested that SCI induced changes in protein synthesis-, neuroplasticity-, and oxidative stress-associated pathways, a subset of which were shown in transcriptomics data to be inosine sensitive. These findings provide insights into the molecular landscape of the bladder following SCI and identify key inosine-sensitive pathways associated with injury.
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Registered trials
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