@article{34748dcf6b8f4506b1a46b7ff171429c,
title = "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 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.",
author = "Chen, {Yi Fan} and Lin, {I. Hsuan} and Guo, {Yu Ru} and Chiu, {Wei Jun} and Wu, {Mai Szu} and Wei Jia and Yun Yen",
note = "Funding Information: The authors acknowledge the technical support (sample preparation for transmission electron microscopy) provided by the TMU Core Facility. The authors also thank the Taiwan Animal Consortium (MOST 106-2319-B-001-004) – Taiwan Mouse Clinic, which is funded by the Ministry of Science and Technology (MOST) of Taiwan, for technical support in monitoring for metabolic cage and biochemical index analyses. This work was financially supported by the “TMU Research Center of Cancer Translational Medicine” from The Featured Areas Research Center Program within the framework of the Higher Education Sprout Project by the Ministry of Education (MOE) in Taiwan. This work was also supported by a Health and welfare surcharge of tobacco products grant (CECR grant: MOHW107-TDU-B-212-114014, MOHW108-TDU-B-212-124026 and MOHW108-TDU-B-212-124020 to Y.Y.). This work was supported by Ministry of Science and Technology (MOST-108-2321-B-038-003 to Y.Y.). This work was also supported by the Ministry of Science and Technology (grant number MOST105-2320-B-038-022-MY3 to Y.F.C.) and Taipei Medical University (Grant Numbers 105TMU-CIT-01-4 and 106TMU-CIT-01-4 to Y.F.C.).",
year = "2019",
month = dec,
day = "1",
doi = "10.1038/s41598-019-49663-3",
language = "English",
volume = "9",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",
number = "1",
}
