Identify new pseudogene RPL7P1-oriented network as a drug target against infections pre-existing diabetes
This research elucidates the potential role of the novel pseudogene RPL7P1 in DCI, highlighting the importance of pseudogenes in complex diseases and providing novel insights into the epigenetic modulation of diabetes complicated by infections. Insight Box Diabetes and infections often coexist, complicating our understanding of their shared mechanisms. To address this, we employed a comprehensive suite of bioinformatics methods, including pathway mapping, ceRNA analysis, PPI evaluation, single-cell dissection, network modeling, and drug repositioning strategies. Our research revealed that RPL7P1 modulates signaling pathways by sponging miR-144-3p, interacting with IGF2BP2 and ATP6V1E1 RNA, and influencing cuproptosis-a novel form of cell death-through m6A modification, a key RNA modification. We identified endothelial cells as key mediators of the RPL7P1 network in the liver. Additionally, our integrative approach uncovered five potential therapeutic drugs targeting the RPL7P1 network. These findings provide novel insights into coexisting diabetes and infections, underscoring the value of multidisciplinary strategies in uncovering coexisting disease mechanisms and treatment opportunities.
Authors
- Ying Wang (ORCID: https://orcid.org/0000-0001-8537-3954)
- Jiajun Chen (ORCID: https://orcid.org/0000-0003-1065-9952)
- Chenxi Li (ORCID: https://orcid.org/0009-0008-6029-7180)
- Shiwei Chen (ORCID: https://orcid.org/0000-0002-4766-6980)
- Xiangqi Li (ORCID: https://orcid.org/0000-0003-2675-0574)
Institutions
- University of Shanghai for Science and Technology (CN)
- Second Military Medical University (CN)
- Shanghai University of Medicine and Health Sciences (CN)
- Shanghai Pudong New Area Gongli Hospital (CN)
Publication Details
- Journal
- Integrative Biology
- Published
- 2025-01-01
- DOI
- https://doi.org/10.1093/intbio/zyaf015
- Primary Topic
- RNA modifications and cancer
- Type
- article
- Field-Weighted Citation Impact
- 0.00