Rrm2b deletion causes mitochondrial metabolic defects in renal tubules

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 whic...

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Autores principales: Yi-Fan Chen, I-Hsuan Lin, Yu-Ru Guo, Wei-Jun Chiu, Mai-Szu Wu, Wei Jia, Yun Yen
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Publicado: Nature Portfolio 2019
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Acceso en línea:https://doaj.org/article/f53ecd6e0971403ab1d3fc73940a2606
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spelling oai:doaj.org-article:f53ecd6e0971403ab1d3fc73940a26062021-12-02T15:09:15ZRrm2b deletion causes mitochondrial metabolic defects in renal tubules10.1038/s41598-019-49663-32045-2322https://doaj.org/article/f53ecd6e0971403ab1d3fc73940a26062019-09-01T00:00:00Zhttps://doi.org/10.1038/s41598-019-49663-3https://doaj.org/toc/2045-2322Abstract 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.Yi-Fan ChenI-Hsuan LinYu-Ru GuoWei-Jun ChiuMai-Szu WuWei JiaYun YenNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 9, Iss 1, Pp 1-12 (2019)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Yi-Fan Chen
I-Hsuan Lin
Yu-Ru Guo
Wei-Jun Chiu
Mai-Szu Wu
Wei Jia
Yun Yen
Rrm2b deletion causes mitochondrial metabolic defects in renal tubules
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.
format article
author Yi-Fan Chen
I-Hsuan Lin
Yu-Ru Guo
Wei-Jun Chiu
Mai-Szu Wu
Wei Jia
Yun Yen
author_facet Yi-Fan Chen
I-Hsuan Lin
Yu-Ru Guo
Wei-Jun Chiu
Mai-Szu Wu
Wei Jia
Yun Yen
author_sort Yi-Fan Chen
title Rrm2b deletion causes mitochondrial metabolic defects in renal tubules
title_short Rrm2b deletion causes mitochondrial metabolic defects in renal tubules
title_full Rrm2b deletion causes mitochondrial metabolic defects in renal tubules
title_fullStr Rrm2b deletion causes mitochondrial metabolic defects in renal tubules
title_full_unstemmed Rrm2b deletion causes mitochondrial metabolic defects in renal tubules
title_sort rrm2b deletion causes mitochondrial metabolic defects in renal tubules
publisher Nature Portfolio
publishDate 2019
url https://doaj.org/article/f53ecd6e0971403ab1d3fc73940a2606
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AT ihsuanlin rrm2bdeletioncausesmitochondrialmetabolicdefectsinrenaltubules
AT yuruguo rrm2bdeletioncausesmitochondrialmetabolicdefectsinrenaltubules
AT weijunchiu rrm2bdeletioncausesmitochondrialmetabolicdefectsinrenaltubules
AT maiszuwu rrm2bdeletioncausesmitochondrialmetabolicdefectsinrenaltubules
AT weijia rrm2bdeletioncausesmitochondrialmetabolicdefectsinrenaltubules
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