Evidence map›Paper›PMID 31519977›Full record

ArticleScientific reports2019

Rrm2b deletion causes mitochondrial metabolic defects in renal tubules.

Yi-Fan Chen, I-Hsuan Lin, Yu-Ru Guo, Wei-Jun Chiu, Mai-Szu Wu, Wei Jia, Yun Yen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.4field-weighted citation impact, top 37% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. RRM2B deficiency causes dATP and dGTP depletion through enhanced degradation and slower synthesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. American journal of cancer research · 2021
    Article
  10. Article
  11. The Dimensions of Primary Mitochondrial Disorders.Frontiers in cell and developmental biology · 2020
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Yi-Fan ChenThe Ph.D. Program for Translational Medicine, College of Medical Science and Technology, Taipei Medical University, 11031, Taipei, Taiwan.
I-Hsuan LinTMU Research Center of Cancer Translational Medicine, Taipei Medical University, 11031, Taipei, Taiwan.ORCID http://orcid.org/0000-0002-6207-1299
Yu-Ru GuoPh.D. Program of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, 11031, Taipei, Taiwan.
Wei-Jun ChiuThe Ph.D. Program for Translational Medicine, College of Medical Science and Technology, Taipei Medical University, 11031, Taipei, Taiwan.
Mai-Szu WuDepartment of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, 11031, Taipei, Taiwan.
Wei JiaCancer Biology Program, University of Hawaii Cancer Center, Honolulu, HI, 96813, USA.ORCID http://orcid.org/0000-0002-3739-8994
Yun YenTMU Research Center of Cancer Translational Medicine, Taipei Medical University, 11031, Taipei, Taiwan. yyen@tmu.edu.tw.
Taipei Medical University · TWTaipei Medical University Hospital · TWTaipei Medical University-Shuang Ho Hospital · TWUniversity of Hawaiʻi at Mānoa · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Oxidative StressAnimalsCell Cycle ProteinsDNA ReplicationFemaleKidney TubulesMiceMice, Inbred C57BLMice, KnockoutMitochondriaOxidation-ReductionRibonucleotide ReductasesCell Cycle ProteinsRibonucleotide ReductasesRrm2b protein, mouse

Identifiers

PMID31519977
PMCPMC6744457
OpenAlexW2973155341

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.