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- Publisher Website: 10.1038/s41598-019-49663-3
- Scopus: eid_2-s2.0-85072168231
- PMID: 31519977
- WOS: WOS:000485680900035
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Article: Rrm2b deletion causes mitochondrial metabolic defects in renal tubules
Title | Rrm2b deletion causes mitochondrial metabolic defects in renal tubules |
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Authors | |
Issue Date | 2019 |
Citation | Scientific Reports, 2019, v. 9, n. 1, article no. 13238 How to Cite? |
Abstract | Renal diseases impose considerable health and economic burdens on health systems worldwide, and there is a lack of efficient methods for the prevention and treatment due to their complexity and heterogeneity. Kidneys are organs with a high demand for energy produced by mitochondria, in which Rrm2b has critical functions as reported. The Rrm2b kidney-specific knockout mice we generated exhibited age-dependent exacerbated features, including mitochondrial dysfunction and increased oxidative stress; additionally, resulted in severe disruption of mitochondria-related metabolism. Rrm2b is vital not only to supply dNTPs for DNA replication and repair, but also to maintain structural integrity and metabolic homeostasis in mitochondria. Thence, Rrm2b deletion might induce chronic kidney defects in mice. This model can facilitate exploration of novel mechanisms and targeted therapies in the kidney diseases and has important translational and clinical implications. |
Persistent Identifier | http://hdl.handle.net/10722/342592 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Chen, Yi Fan | - |
dc.contributor.author | Lin, I. Hsuan | - |
dc.contributor.author | Guo, Yu Ru | - |
dc.contributor.author | Chiu, Wei Jun | - |
dc.contributor.author | Wu, Mai Szu | - |
dc.contributor.author | Jia, Wei | - |
dc.contributor.author | Yen, Yun | - |
dc.date.accessioned | 2024-04-17T07:04:53Z | - |
dc.date.available | 2024-04-17T07:04:53Z | - |
dc.date.issued | 2019 | - |
dc.identifier.citation | Scientific Reports, 2019, v. 9, n. 1, article no. 13238 | - |
dc.identifier.uri | http://hdl.handle.net/10722/342592 | - |
dc.description.abstract | Renal diseases impose considerable health and economic burdens on health systems worldwide, and there is a lack of efficient methods for the prevention and treatment due to their complexity and heterogeneity. Kidneys are organs with a high demand for energy produced by mitochondria, in which Rrm2b has critical functions as reported. The Rrm2b kidney-specific knockout mice we generated exhibited age-dependent exacerbated features, including mitochondrial dysfunction and increased oxidative stress; additionally, resulted in severe disruption of mitochondria-related metabolism. Rrm2b is vital not only to supply dNTPs for DNA replication and repair, but also to maintain structural integrity and metabolic homeostasis in mitochondria. Thence, Rrm2b deletion might induce chronic kidney defects in mice. This model can facilitate exploration of novel mechanisms and targeted therapies in the kidney diseases and has important translational and clinical implications. | - |
dc.language | eng | - |
dc.relation.ispartof | Scientific Reports | - |
dc.title | Rrm2b deletion causes mitochondrial metabolic defects in renal tubules | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1038/s41598-019-49663-3 | - |
dc.identifier.pmid | 31519977 | - |
dc.identifier.scopus | eid_2-s2.0-85072168231 | - |
dc.identifier.volume | 9 | - |
dc.identifier.issue | 1 | - |
dc.identifier.spage | article no. 13238 | - |
dc.identifier.epage | article no. 13238 | - |
dc.identifier.eissn | 2045-2322 | - |
dc.identifier.isi | WOS:000485680900035 | - |