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.

Original languageEnglish
Number of pages1
JournalScientific Reports
Volume9
Issue number1
DOIs
Publication statusPublished - Sep 13 2019

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Kidney
Mitochondria
Kidney Diseases
DNA Replication
Knockout Mice
DNA Repair
Oxidative Stress
Homeostasis
Economics
Health
Therapeutics
Global Health

ASJC Scopus subject areas

  • General

Cite this

Rrm2b deletion causes mitochondrial metabolic defects in renal tubules. / Chen, Yi Fan; Lin, I. Hsuan; Guo, Yu Ru; Chiu, Wei Jun; Wu, Mai Szu; Jia, Wei; Yen, Yun.

In: Scientific Reports, Vol. 9, No. 1, 13.09.2019.

Research output: Contribution to journalArticle

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AU - Chiu, Wei Jun

AU - Wu, Mai Szu

AU - Jia, Wei

AU - Yen, Yun

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